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Article in English | WPRIM | ID: wpr-878319


Objective@#Epidemiological studies reveal that exposure to fine particulate matter (aerodynamic diameter ≤ 2.5 μm, PM @*Methods@#EVs were isolated from the serum of healthy subjects, quantified @*Results@#PM @*Conclusions@#EVs treatment promotes cell survival and attenuates PM

A549 Cells , Air Pollutants/toxicity , Apoptosis/drug effects , Cell Survival/drug effects , Extracellular Vesicles , Humans , Male , Middle Aged , Particulate Matter/toxicity , Protective Agents/pharmacology , Proto-Oncogene Proteins c-akt/metabolism , Serum
Braz. j. otorhinolaryngol. (Impr.) ; 86(1): 30-37, Jan.-Feb. 2020. tab, graf
Article in English | LILACS | ID: biblio-1089360


Abstract Introduction Ototoxicity is a health problem appearing after powerful treatments in serious health conditions. It is sometimes inevitable when treatment of the serious disease is required. Cisplatin is an antineoplastic agent which was investigated previously to reveal increased nitrogen and reactive oxygen radicals that damages hair cells, resulting in ototoxicity. N-acetylcysteine, previously shown to decrease ototoxicity caused by different agents, is known to be a powerful in vitro antioxidant. Probably N-acetylcysteine, in addition to its antioxidant effect, blocks a cascade where reactive oxygen species result in apoptosis in the cochlea. Objectives The possible preventive effect of N-acetylcysteine in cisplatin ototoxicity was studied with auditory brain stem responses, otoacoustic emissions, and histopathological investigation of the cochlea in a scanning electron microscopy. Methods This study was conducted on 21 Wistar Albino rats in four groups. 1 mL/kg/day three times in total intraperitoneal (i.p.) Saline (n = 5), 500 mg/kg/day i.p. three times in total N-acetylcysteine (n = 5), i.p. 15 mg/kg cisplatin alone (single dose) (n = 5) and i.p. 15 mg/kg cisplatin plus 500 mg/kg/day N-acetylcysteine (n = 6) were administered. The rats were anesthetized to study the hearing tests before and after the experiment. The rats were sacrificed to investigate the cochleas by scanning electron microscopy. Results Auditory brain stem responses and otoacoustic emissions values were attenuated in the cisplatin group. The group that received N-acetylcysteine in addition to cisplatin had better auditory brain stem responses thresholds and otoacoustic emissions. The samples obtained from the cisplatin group showed surface irregularities, degeneration areas, and total or partial severe stereocilia losses. The changes were milder in the cisplatin + N-acetylcysteine group. Conclusion Cisplatin ototoxicity can be detected by auditory brain stem responses and otoacoustic emissions testing in rats. N-acetylcysteine may protect the cochlear cells from histopathological changes. We concluded that N-acetylcysteine given 4 h after cisplatin injection has a potential otoprotective effect against cisplatin ototoxicity. which suggests it could be used in clinical trials.

Resumo Introdução A ototoxicidade é um problema que pode ocorrer após certos tipos de tratamentos para condições graves de saúde. Às vezes é inevitável quando o tratamento da doença é necessário. A cisplatina é um agente antineoplásico cujo uso em pesquisas anteriores demonstrou aumentar os radicais livres de nitrogênio e espécies reativas de oxigênio que danificam as células ciliadas e resultam em ototoxicidade. Por outro lado, a N-acetilcisteína, que já demonstrou diminuir a ototoxicidade causada por diferentes agentes, é conhecida por ser um potente antioxidante in vitro. Provavelmente a N-acetilcisteína, além de seu efeito antioxidante, bloqueia uma cascata onde espécies reativas de oxigênio resultam em apoptose na cóclea. Objetivos Estudar o possível efeito preventivo da N-acetilcisteína na ototoxicidade por cisplatina por meio de potencial evocado auditivo de tronco encefálico, emissões otoacústicas e investigação histopatológica da cóclea por microscopia eletrônica de varredura. Método Este estudo foi realizado em 21 ratos albinos Wistar, separados em quatro grupos. Foram administrados: 1 mL/kg/dia intraperitoneal (i.p.) de solução salina (n = 5), três vezes no total; 500 mg/kg/dia i.p. de N-acetilcisteína (n = 5), três vezes no total; 15 mg/kg i.p. (dose única) somente de cisplatina (n = 5) e 15 mg/kg i.p. de cisplatina e 500 mg/kg/dia i.p. de N-acetilcisteína (n = 6). Os ratos foram anestesiados para estudo dos testes auditivos antes e depois do experimento. Os ratos foram sacrificados para investigação da cóclea por microscopia eletrônica de varredura. Resultados Os potenciais evocados auditivos de tronco encefálico e os valores das emissões otoacústicas estavam atenuados no grupo cisplatina. O grupo que recebeu N-acetilcisteína além da cisplatina apresentou melhores limiares de respostas auditivas do tronco encefálico e emissões otoacústicas. As amostras obtidas do grupo cisplatina apresentaram irregularidades de superfície, áreas de degeneração, com perdas graves totais ou parciais de estereocílios. As alterações foram mais leves no grupo cisplatina + N-acetilcisteína. Conclusão A ototoxicidade por cisplatina pode ser detectada por meio de potenciais evocados auditivos de tronco encefálico e pelo teste de emissões otoacústicas em ratos. A N-acetilcisteína pode proteger as células cocleares contra alterações histopatológicas. Concluímos que a N-acetilcisteína administrada 4 horas após a injeção de cisplatina tem potencial efeito otoprotetor contra a ototoxicidade por cisplatina e pode ser utilizada em ensaios clínicos.

Animals , Male , Acetylcysteine/administration & dosage , Cisplatin/adverse effects , Protective Agents/administration & dosage , Ototoxicity/etiology , Antineoplastic Agents/adverse effects , Antioxidants/administration & dosage , Acetylcysteine/pharmacology , Microscopy, Electron, Scanning , Evoked Potentials, Auditory, Brain Stem , Rats, Wistar , Cochlea/pathology , Apoptosis , Hair Cells, Auditory, Outer/drug effects , Hair Cells, Auditory, Outer/pathology , Protective Agents/pharmacology , Disease Models, Animal , Stereocilia/drug effects , Stereocilia/pathology , Ototoxicity/prevention & control , Hearing Tests , Antioxidants/pharmacology
Braz. j. med. biol. res ; 53(10): e9183, 2020. tab, graf
Article in English | LILACS, ColecionaSUS | ID: biblio-1132479


H1N1 virus-induced excessive inflammatory response contributes to severe disease and high mortality rates. There is currently no effective strategy against virus infection in lung. The present study evaluated the protective roles of a natural compound, lapiferin, in H1N1 virus-induced pulmonary inflammation in mice and in cultured human bronchial epithelial cells. Initially, Balb/C mice were grouped as Control, H1N1 infection (intranasally infected with 500 plaque-forming units of H1N1 virus), lapiferin (10 mg/kg), and H1N1+lapiferin (n=10/group). Lung histology, expression of inflammatory factors, and survival rates were assessed after 14 days of exposure. Administration of lapiferin significantly alleviated the virus-induced inflammatory infiltrate in lung tissues. Major pro-inflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, were decreased at both mRNA and protein levels by lapiferin administration in the lung homogenate. Lapiferin also reduced inflammatory cell numbers in bronchoalveolar fluid. Mechanistically, lapiferin suppressed the transcriptional activity and protein expression of NF-κB p65, causing inhibition on NF-κB signaling. Pre-incubation of human bronchial epithelial cells with an NF-κB signaling specific activator, ceruletide, significantly blunted lapiferin-mediated inhibition of pro-inflammatory cytokines secretion in an air-liquid-interface cell culture experiment. Activation of NF-κB signaling also blunted lapiferin-ameliorated inflammatory infiltrate in lungs. These results suggested that lapiferin was a potent natural compound that served as a therapeutic agent for virus infection in the lung.

Humans , Animals , Rabbits , Pneumonia , Sesquiterpenes/pharmacology , NF-kappa B/metabolism , Protective Agents/pharmacology , Influenza A Virus, H1N1 Subtype , Signal Transduction , Cytokines , Inflammation
J. bras. nefrol ; 41(3): 315-322, July-Sept. 2019. tab, graf
Article in English | LILACS | ID: biblio-1040245


Abstract Introduction: It is hypothesized that increased macrophage migration inhibitory factor (MIF) expression may contribute to diabetic nephropathy (DN) pathogenesis. The aim of the present study was to investigate the renal effects of MIF inhibition in a diabetic experimental model. Methods: Eighteen male Wistar rats (230 ± 20 g) were divided into three groups: 1) control, 2) diabetic (STZ, 50 mg/kg, dissolved in saline, ip), 3) diabetic + MIF antagonist (p425, 1 mg/kg per day, ip, on the 21th day, for 21 consecutive days). The treatment started since we founwd a significant increase in urine albumin excretion (UAE) rate in the diabetic rats in comparison with the control rats. The rats were kept individually in metabolic cages (8 AM-2 PM) and urine samples were collected in the 21 and 42th day. At the end, blood and tissue samples were collected for biochemical (BS, UPE, urine GAG, BUN, Cr, Na, and K) and histological analyses. Results: The results of this study showed that MIF antagonist (p425) significantly decreased urine protein and GAG excretion, urine protein/creatinine ratio, and serum BUN and Cr in the streptozotocin-induced DN in the rats. Pathological changes were significantly alleviated in the MIF antagonist (p425)-administered DN rats. Conclusion: Collectively, these data suggested that MIF antagonist (p425) was able to protect against functional and histopathological injury in the DN.

Resumo Introdução: Supõe-se que elevações da expressão do fator de inibição da migração de macrófagos (MIF) possam contribuir para a patogênese da nefropatia diabética (ND). O objetivo do presente estudo foi investigar os efeitos renais da inibição do MIF em um modelo experimental diabético. Métodos: Dezoito ratos Wistar machos (230 ± 20g) foram divididos em três grupos: 1) controle, 2) diabético (STZ 50 mg/kg dissolvida em soro fisiológico, IP), 3) diabético + antagonista do MIF (p425 1 mg/kg por dia IP no 21o dia por 21 dias consecutivos). O tratamento começou após a identificação de aumento significativo na albuminúria nos ratos diabéticos em relação aos controles. Os ratos foram mantidos individualmente em gaiolas metabólicas (8h-14h) e amostras de urina foram colhidas no 21o e no 42o dia. Ao final do estudo, amostras de sangue e tecido foram colhidas para análises bioquímicas (BS, excreção urinária de proteína, excreção urinária de GAGs, BUN, Cr, Na e K) e histológicas. Resultados: O presente estudo demonstrou que o antagonista do MIF (p425) diminuiu significativamente proteinúria, excreção urinária de GAGs , relação proteína/creatinina na urina, BUN e Cr no grupo com ND induzida por estreptozotocina. As alterações patológicas foram significativamente abrandadas nos ratos com ND que receberam antagonista do MIF (p425). Conclusão: Coletivamente, os dados sugerem que o antagonista do MIF (p425) teve efeito protetor contra lesões funcionais e histopatológicas da ND.

Animals , Male , Rats , Macrophage Migration-Inhibitory Factors/antagonists & inhibitors , Intramolecular Oxidoreductases/antagonists & inhibitors , Protective Agents/therapeutic use , Protective Agents/pharmacology , Diabetes Mellitus, Experimental/pathology , Diabetic Nephropathies/therapy , Blood Glucose , Rats, Wistar , Streptozocin/pharmacology , Creatinine/urine , Creatinine/blood , Diabetes Mellitus, Experimental/chemically induced , Diabetes Mellitus, Experimental/urine , Diabetes Mellitus, Experimental/blood , Diabetic Nephropathies/urine , Diabetic Nephropathies/pathology , Diabetic Nephropathies/blood , Albuminuria/drug therapy , Disease Models, Animal , Glycosaminoglycans/urine , Kidney/pathology , Macrophage Activation
Rev. Assoc. Med. Bras. (1992) ; 65(9): 1193-1200, Sept. 2019. graf
Article in English | LILACS | ID: biblio-1041079


SUMMARY OBJECTIVES This study was conducted to reveal the possible protective effects of ticagrelor and enoxaparin pretreatment against ischemia-reperfusion (IR)-induced injury on the lung tissue of a rat model. METHODS Wistar albino rats were randomly divided into 4 groups as follows: group-1 (control-sham), group-2 (control-saline+IR), group-3 (ticagrelor+IR), group-4 (enoxaparin+IR). Before the ischemic period, saline, ticagrelor, and enoxaparin were administered to the 2nd-4th groups, respectively. In these groups, IR injury was induced by clamping the aorta infrarenally for 2 h, followed by 4 h of reperfusion except group-1. After the rats were euthanized, the lungs were processed for histological examinations. Paraffin sections were stained with Haematoxylin&Eosin (H&E) for light microscopic observation. Apoptosis was evaluated by caspase-3 immunoreactivity. Data were statistically analyzed using the SPSS software. RESULTS In the lung sections stained with H&E, a normal histological structure was observed in group-1, whereas disorganized epithelial cells, hemorrhage, and inflammatory cell infiltration were seen in the alveolar wall in group-2. The histologic structure of the treatment groups was better than that of group-2. Caspase-3(+) apoptotic cells were noticeable in sections of group-2 and were lower in the treatment groups. In group-4, caspase-3 immunostaining was lower than in group-3. In group-2, apoptotic cells were significantly higher than in the other groups (p<0.001). CONCLUSION Based on the histological results, we suggested that both therapies ameliorated the detrimental effects of IR. Caspase-3 immunohistochemistry results also revealed that pre-treatment with enoxaparin gave better results in an IR-induced rat injury model. In further studies, other parameters such as ROS and inflammatory gene expressions should be evaluated for accurate results.

RESUMO OBJETIVOS Este estudo foi realizado para revelar os possíveis efeitos protetores do ticagrelor e do pré-tratamento da enoxaparina no tecido pulmonar contra o modelo de lesão induzida por isquemia-reperfusão (IR). MÉTODOS Ratos albinos Wistar foram randomizados e divididos em quatro grupos: grupo 1 (controle-sham), grupo 2 (controle-salina + IR), grupo 3 (ticagrelor + IR), grupo 4 (enoxaparina + IR). Antes do período isquêmico, salina, ticagrelor e enoxaparina foram administrados nos grupos 2-4, respectivamente. Nesses grupos, a lesão de IR foi induzida pelo clampeamento da aorta na região da infrarrenal por duas horas, seguida por quatro horas de reperfusão, exceto no grupo 1. Após a sacrificação, os pulmões foram processados para exames histológicos. Secções de parafina foram coradas com hematoxilina e eosina (H&E) para observação microscópica de luz. A apoptose foi avaliada pela imunorreatividade da caspase-3. Os dados foram analisados estatisticamente pelo programa SPSS. RESULTADOS Nas secções pulmonares coradas com H&E, estrutura histológica normal foi observada no grupo 1, enquanto células epiteliais desorganizadas, hemorragia e infiltração de células inflamatórias foram observadas na parede alveolar no grupo 2. A estrutura histológica dos grupos de tratamento foi melhor que o grupo 2. Células apoptóticas caspase-3 (+) foram notadas em secções do grupo 2, e essas células foram mais baixas nos grupos de tratamento. No grupo 4, a imunocoloração com caspase-3 foi menor que no grupo 3. No grupo 2, as células apoptóticas foram significativamente maiores que nos outros grupos (p<0,001). CONCLUSÃO Com base nos resultados histológicos, sugerimos que ambas as terapias atenuaram os efeitos prejudiciais da RI. Resultados de imuno-histoquímica com caspase-3 também revelaram que o pré-tratamento com enoxaparina proporcionou melhores resultados no modelo de lesão induzida por IR. Em estudos posteriores, outros parâmetros, como ROS e expressões gênicas inflamatórias, devem ser avaliados quanto a resultados precisos.

Animals , Male , Aorta, Abdominal/surgery , Reperfusion Injury/prevention & control , Enoxaparin/pharmacology , Protective Agents/pharmacology , Ticagrelor/pharmacology , Lung/drug effects , Reperfusion Injury/pathology , Random Allocation , Rats, Wistar , Apoptosis/drug effects , Disease Models, Animal , Caspase 3/metabolism , Lung Injury/prevention & control , Lung/pathology
Arq. bras. oftalmol ; 82(4): 310-316, July-Aug. 2019. graf
Article in English | LILACS | ID: biblio-1019421


ABSTRACT Purpose: Chronic instillation of benzalkonium chloride, a preservative, has inflammatory effects on the ocular surface. However, addition of the anti-inflammatory agent cyclosporine to a therapeutic protocol may mitigate these effects. This study compared the toxic effects of a 0.1% benzalkonium chloride solution and the possible protective effect of 0.05% cyclosporine when applied topically to the rabbit conjunctiva. Methods: Fifteen age- and weight-matched, female New Zealand white rabbits were categorized into three groups and treated for 30 consecutive days. Group 1, 2, and 3 - benzalkonium chloride received 0.1% every 24 h, 0.05% cyclosporine every 6 h, and both treatments, respectively. In each rabbit, the left eye was subjected to treatment and the right eye was a control. The rabbits were euthanized at after the experiment. Goblet cells and blood vessels were then enumerated in conjunctival tissues stained with periodic acid-Schiff and hematoxylin-eosin, respectively. Differences between treated and untreated eyes and between groups were compared using the t-test and analysis of variance. Results: Benzalkonium chloride treatment, with and without cyclosporine, significantly reduced (p≤0.05) in the number of goblet cells in treatment eyes compared with that in respective control eyes. Alternatively, adding cyclosporine to benzalkonium chloride did not prevent the loss of conjunctival goblet cells, and a significant reduction in the number of goblet cells was noted. Benzalkonium chloride-induced significant increase in the number of new blood vessels was mitigated significantly by the addition of cyclosporine. Conclusion: This study demonstrated the magnitude of conjunctival injury caused by chronic instillation of benzalkonium chloride. Although cyclosporine did not mitigate the effects on goblet cells, its addition minimized inflammatory angiogenesis induced by benzalkonium chloride.

RESUMO Objetivo: A instilação crônica de cloreto de benzal­cônio, um conservante, tem efeitos inflamatórios na superfície ocular. No entanto, a adição do agente anti-inflamatório ciclosporina a um protocolo terapêutico pode atenuar esses efeitos. Este estudo comparou os efeitos tóxicos de uma solução de cloreto de benzalcônio a 0,1% e o possível efeito protetor de ciclosporina a 0,05% quando aplicado topicamente à conjuntiva de coelho. Métodos: Quinze coelhos fêmeas brancos da raça Nova Zelândia, pareados por idade e peso, foram categorizados em três grupos e tratados por 30 dias consecutivos. Os grupos 1, 2 e 3 - receberam cloreto de benzalcônio 0,1% a cada 24h, ciclosporina a 0,005% a cada 6h e ambos os tratamentos, respectivamente. Em cada coelho, o olho esquerdo foi submetido a tratamento e o olho direito foi controle. Os coelhos foram submetidos à eutanásia após o experimento. Células caliciformes e vasos sanguíneos foram então enumerados em tecidos conjuntivais corados com ácido periódico-Schiff e hematoxilina-eosina, respectivamente. As diferenças entre os olhos tratados e não tratados e entre os grupos foram comparadas usando o teste t e análise de variância. Resultados: O tratamento com cloreto de benzalcônio, com e sem ciclosporina, reduziu significativamente (p£0,05) o número de células caliciformes nos olhos tratados em comparação com os olhos controle correspondentes. Alternativamente, a adição de ciclosporina ao cloreto de benzalcônio não impediu a perda de células caliciformes conjuntivais, e foi observada uma redução significativa no número de células caliciformes. O aumento significativo induzido pelo cloreto de benzalcônio no número de novos vasos sanguíneos foi significativamente mitigado pela adição da ciclosporina. Conclusão: Este estudo demonstrou a magnitude da lesão conjuntival resultante da instilação crônica de cloreto de benzalcônio. Embora a ciclosporina não tenha atenuado os efeitos nas células caliciformes, sua adição minimizou a angiogênese inflamatória induzida pelo cloreto de benzalcônio.

Animals , Female , Rats , Preservatives, Pharmaceutical/adverse effects , Benzalkonium Compounds/adverse effects , Cyclosporine/pharmacology , Conjunctiva/drug effects , Protective Agents/pharmacology , Anti-Inflammatory Agents/pharmacology , Time Factors , Random Allocation , Reproducibility of Results , Treatment Outcome , Conjunctiva/pathology , Goblet Cells/drug effects , Angiogenesis Inducing Agents/pharmacology
Rev. bras. anestesiol ; 69(2): 160-167, Mar.-Apr. 2019. graf
Article in English | LILACS | ID: biblio-1003397


Abstract Background and objectives: Dexmedetomidine has demonstrated protective effects against lung injury in vitro. Here, we investigated whether dexmedetomidine preconditioning protected against lung injury in hemorrhagic shock rats. Methods: Male Sprague-Dawley rats were randomly divided into four groups (n = 8): control group, hemorrhagic shock group, 5 dexmedetomidine (DEX1) group, and 10 dexmedetomidine (DEX2) group. Saline or dexmedetomidine were administered over 20 min. 30 min after injection, hemorrhage was initiated in the hemorrhagic shock, DEX1 and DEX2 group. Four hours after resuscitation, protein and cellular content in bronchoalveolar lavage fluid, and the lung histopathology were measured. The malondialdehyde, superoxide dismutase, Bcl-2, Bax and caspase-3 were also tested in the lung tissue. Results: Compare with hemorrhagic shock group, 5 dexmedetomidine pretreatment reduced the apoptosis (2.25 ± 0.24 vs. 4.12 ± 0.42%, p < 0.05), histological score (1.06 ± 0.12 vs. 1.68 ± 0.15, p < 0.05) and protein (1.92 ± 0.38 vs. 3.95 ± 0.42 mg.mL-1, p < 0.05) and WBC (0.42 ± 0.11 vs. 0.92 ± 0.13 × 109/L, p < 0.05) in bronchoalveolar lavage fluid. Which is correlated with increased superoxide dismutase activity (8.35 ± 0.68 vs. 4.73 ± 0.44 protein, p < 0.05) and decreased malondialdehyde (2.18 ± 0.19 vs. 3.28 ± 0.27 protein, p < 0.05). Dexmedetomidine preconditioning also increased the Bcl-2 level (0.55 ± 0.04 vs. 0.34 ± 0.05, p < 0.05) and decreased the level of Bax (0.46 ± 0.03 vs. 0.68 ± 0.04, p < 0.05), caspase-3 (0.49 ± 0.03 vs. 0.69 ± 0.04, p < 0.05). However, we did not observe any difference between the DEX1 and DEX2 groups for these (p > 0.05). Conclusion: Dexmedetomidine preconditioning has a protective effect against lung injury caused by hemorrhagic shock in rats. The potential mechanisms involved are the inhibition of cell death and improvement of antioxidation. But did not show a dose-dependent effect.

Resumo Justificativa e objetivos: Dexmedetomidina demonstrou efeitos protetores contra a lesão pulmonar in vitro. Neste estudo, investigamos se o pré-condicionamento com dexmedetomidina protege contra a lesão pulmonar em ratos com choque hemorrágico. Métodos: Ratos machos, Sprague-Dawley, foram aleatoriamente divididos em quatro grupos (n = 8): grupo controle, grupo com choque hemorrágico, grupo com 5 µ de dexmedetomidina (DEX1) e grupo com 10 µ de dexmedetomidina (DEX2). Solução salina ou dexmedetomidina foi administrada durante 20 minutos. Trinta minutos após a injeção, a hemorragia foi iniciada nos grupos choque hemorrágico, DEX1 e DEX2. Quatro horas após a ressuscitação, a proteína e o conteúdo celular no lavado broncoalveolar e a histopatologia pulmonar foram medidos. Malondialdeído, superóxido dismutase, Bcl-2, Bax e caspase-3 também foram testados no tecido pulmonar. Resultados: Na comparação com o grupo choque hemorrágico, o pré-tratamento com 5 de dexmedetomidina reduziu a apoptose (2,25 ± 0,24 vs. 4,12 ± 0,42%, p < 0,05), escore histológico (1,06 ± 0,12 vs. 1,68 ± 0,15, p < 0,05) e proteína (1,92 ± 0,38 vs. 3,95 ± 0,42 mg.mL-1, p < 0,05) e leucócitos (0,42 ± 0,11 vs. 0,92 ± 0,13 × 109/L, p < 0,05) no lavado broncoalveolar; o que está correlacionado com o aumento da atividade da superóxido dismutase (8,35 ± 0,68 vs. 4,73 ± 0,44 de proteína, p < 0,05) e diminuição do malondialdeído (2,18 ± 0,19 vs. 3,28 ± 0,27 de proteína, p < 0,05). O pré-condicionamento com dexmedetomidina também aumentou o nível de Bcl-2 (0,55 ± 0,04 vs. 0,34 ± 0,05, p < 0,05) e diminuiu o nível de Bax (0,46 ± 0,03 vs. 0,68 ± 0,04, p < 0,05), caspase-3 (0,49 ± 0,03 vs. 0,69 ± 0,04, p < 0,05). No entanto, não houve diferença entre os grupos DEX1 e DEX2 para essas proteínas (p > 0,05). Conclusão: O pré-condicionamento com dexmedetomidina tem um efeito protetor contra a lesão pulmonar causada por choque hemorrágico em ratos. Os potenciais mecanismos envolvidos são a inibição da morte celular e a melhora da antioxidação. Porém, não mostrou um efeito dose-dependente.

Animals , Male , Rats , Shock, Hemorrhagic/drug therapy , Protective Agents/administration & dosage , Dexmedetomidine/administration & dosage , Lung Injury/prevention & control , Rats , Shock, Hemorrhagic/complications , Bronchoalveolar Lavage Fluid , Rats, Sprague-Dawley , Apoptosis/drug effects , Protective Agents/pharmacology , Dexmedetomidine/pharmacology , Disease Models, Animal , Dose-Response Relationship, Drug , Lung Injury/etiology
Arq. bras. cardiol ; 112(2): 173-178, Feb. 2019. tab, graf
Article in English | LILACS | ID: biblio-983835


Abstract Background: Trimetazidine (TMZ) is an anti-ischemic drug. In spite of its protective effects on cardiovascular system, there is no scientific study on the usefulness of TMZ treatment for prolonged QT interval and cardiac hypertrophy induced by diabetes. Objectives: To evaluate the effects of TMZ on QT interval prolongation and cardiac hypertrophy in the diabetic rats. Methods: Twenty-four male Sprague-Dawley rats (200-250 g) were randomly assigned into three groups (n = 8) by simple random sampling method. Control (C), diabetic (D), and diabetic administrated with TMZ at 10 mg/kg (T10). TMZ was administrated for 8 weeks. The echocardiogram was recorded before isolating the hearts and transfer to a Langendorff apparatus. Hemodynamic parameters, QT and corrected QT interval (QTc) intervals, heart rate and antioxidant enzymes were measured. The hypertrophy index was calculated. The results were evaluated by one-way ANOVA and paired t-test using SPSS (version 16) and p < 0.05 was regarded as significant. Results: The diabetic rats significantly indicated increased hypertrophy, QT and QTc intervals and decreased Left ventricular systolic pressure (LVSP), Left ventricular developed pressure (LVDP), rate pressure product (RPP), Max dp/dt, and min dp/dt (±dp/dt max), heart rate, superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase in the heart. Treatment with TMZ in the diabetic animals was significantly improved these parameters in comparison to the untreated diabetic group. Conclusions: TMZ improves QTc interval prolongation and cardiac hypertrophy in diabetes.

Resumo Fundamento: A trimetazidina (TMZ) é uma droga anti-isquêmica. Apesar de seus efeitos protetores sobre o sistema cardiovascular, não há estudos científicos sobre a utilidade do tratamento com TMZ para o intervalo QT prolongado e a hipertrofia cardíaca induzida pelo diabetes. Objetivo: Avaliar os efeitos da TMZ no prolongamento do intervalo QT e na hipertrofia cardíaca em ratos diabéticos. Métodos: Vinte e quatro ratos machos Sprague-Dawley (200-250 g) foram distribuídos aleatoriamente em três grupos (n = 8) pelo método de amostragem aleatória simples. Controle (C), diabético (D) e diabético administrado com TMZ a 10 mg/kg (T10). A TMZ foi administrada por 8 semanas. O ecocardiograma foi registrado antes de isolar os corações e transferir para um aparelho de Langendorff. Foram medidos os parâmetros hemodinâmicos, intervalo QT e intervalo QT corrigido (QTc), frequência cardíaca e enzimas antioxidantes. O índice de hipertrofia foi calculado. Os resultados foram avaliados pelo one-way ANOVA e pelo teste t pareado pelo SPSS (versão 16) e p < 0,05 foi considerado significativo. Resultados: Os ratos diabéticos indicaram hipertrofia aumentada, intervalos QT e QTc e diminuição da pressão sistólica no ventrículo esquerdo (PSVE), pressão desenvolvida no ventrículo esquerdo (PDVE), duplo produto (DP), Max dp/dt e min dp/dt (± dp/dt max), frequência cardíaca, superóxido dismutase (SOD), glutationa peroxidase (GPx) e catalase no coração. O tratamento com TMZ nos animais diabéticos melhorou significativamente esses parâmetros em comparação com o grupo diabético não tratado. Conclusões: A TMZ melhora o prolongamento do intervalo QTc e a hipertrofia cardíaca no diabetes.

Animals , Male , Trimetazidine/pharmacology , Long QT Syndrome/drug therapy , Cardiomegaly/drug therapy , Protective Agents/pharmacology , Diabetes Complications/drug therapy , Superoxide Dismutase/analysis , Time Factors , Long QT Syndrome/enzymology , Long QT Syndrome/physiopathology , Echocardiography , Catalase/analysis , Random Allocation , Reproducibility of Results , Rats, Sprague-Dawley , Cardiomegaly/enzymology , Cardiomegaly/etiology , Cardiomegaly/physiopathology , Diabetes Complications/enzymology , Diabetes Complications/physiopathology , Diabetes Mellitus, Experimental/complications , Diabetes Mellitus, Experimental/physiopathology , Glutathione Peroxidase/analysis , Hemodynamics/drug effects
Acta cir. bras ; 34(9): e201900901, 2019. tab
Article in English | LILACS | ID: biblio-1054695


Abstract Purpose: To evaluate the effects of tadalafil (TD) in preventing histological alterations of the corpus cavernosum caused by isolated lesions of cavernous nerve (ILCN) and artery (ILCA) in rats. Methods: Fifty male Wistar rats were randomly assigned in five groups: G1: control; G2: bilateral ILCN; G3: bilateral ILCA; G4: ILCN+TD; G5: ILCA+TD. The cavernous bodies were submitted to histomorphometry, immunohistochemistry and biochemical analysis. Results: Nerve density was significantly higher in G2 and G4 compared to control (22.62±2.84 and 19.53±3.47 vs. 15.72±1.82; respectively, p<0.05). Smooth muscle density was significantly lower in G2 and G3 in comparison to G1 (12.87±1.90 and 18.93±1.51 vs. 21.78±1.81, respectively; p<0.05). A significant decrease in the sinusoidal lumen area was observed in G2 compared to controls (5.01±1.62 vs. 9.88±3.66, respectively; p<0.05) and the blood vessel density was increased in G2 and G3 (29.32±4.13 e 20.80±2.47 vs. 10.13±2.71, p<0.05). Collagen density was higher in G3 compared to G1 (93.76±15.81 vs. 64.59±19.25; p<0.05). Conclusions: Histomorphometric alterations caused by ILCN were more intense than those produced by vascular injury, but the collagen analyses showed more fibrosis in animals with ILCA. TD was effective in preventing the majority of the alterations induced by the periprostatic bundle injury.

Animals , Male , Penis/innervation , Penis/blood supply , Protective Agents/pharmacology , Phosphodiesterase 5 Inhibitors/pharmacology , Peripheral Nerve Injuries/prevention & control , Tadalafil/pharmacology , Penis/drug effects , Penis/pathology , Prostatectomy/adverse effects , Immunohistochemistry , Random Allocation , Reproducibility of Results , Collagen/analysis , Collagen/drug effects , Rats, Wistar , Elastic Tissue/anatomy & histology , Elastic Tissue/drug effects , Erectile Dysfunction/prevention & control
Rev. peru. med. integr ; 4(3): 76-82, 2019. tab
Article in Spanish | LILACS, MTYCI | ID: biblio-1146103


Objetivo. Verificar el efecto protector del extracto acuoso de hojas y tallos de Desmodium molliculum EAM (manayupa), en la toxicidad hepática inducida por el naproxeno en ratas Ratus novergicus variedad Wistar albino, hembras. Materiales y métodos. Estudio experimental. Se utilizaron 36 ratas hembras de 250 ± 10 g, divididas en seis grupos de seis: A (control -); B (control + naproxeno); patrón C (silimarina 100 mg / kg) y 3 experimental (EAM): D 80 mg/kg; E 160 mg/kg y F 240 mg/kg). Los grupos B, C, D, E, F recibieron por vía oral naproxeno 27,38 mg, los primeros cinco días y durante 14 días. El efecto protector hepático se determinó mediante el análisis bioquímico: GOT, GPT, GGT, proteínas totales, albúmina sérica, fosfatasa alcalina y creatinina. Resultados. Se encontró que el grupo B perdió peso (180,65 ± 6,5 g), bilirrubina total (0,76 ± 0,4) bilirrubina directa (1.7 ± 0,8), TGO (160 ± 10,4) y TGP (412 ± 20,4) alto, comparado con el grupo A, C, D, E y F. Conclusiones. El EAM tiene efecto protector sobre la toxicidad hepática inducida por naproxeno en ratas, evidenciado por los parámetros bioquímicos.

Objective. To verify the protective effect of the aqueous extract of leaves and stems of Desmodium molliculum EAM (manayupa), on the hepatic toxicity induced by Naproxen in rats Ratus novergicus albino Wistar variety, females. Materials and methods. 36 female rats of 250 ± 10 g were used, divided into six groups of six: A (Control -), B (Control + Naproxen), Pattern C (Silymarin 100 mg / kg) and 3 Experimental (EAM): D 80 mg / kg, E 160 mg / kg and F 240 mg / kg). Groups B, C, D, E, F orally received Naproxen 27.38 mg, the first five days and for 14 days. The hepatic protective effect was determined by the biochemical analysis: GOT, GPT, GGT, total proteins, serum albumin, alkaline phosphatase, creatinine. Results. group B was found to lose weight (180.65 ± 6.5 g), total bilirubin (0.76 ± 0.4) direct bilirubin (1.7 ± 0.8), TGO (160 ± 10.4) and TGP (412 ± 20.4) high, compared to group A, C, D, E and F. Conclusion. EAM has a protective effect on hepatic toxicity induced by naproxen in rats, evidenced by biochemical parameters.

Animals , Female , Rats , Naproxen , Fabaceae/chemistry , Liver/drug effects , Plant Extracts , Protective Agents/pharmacology , Animal Experimentation , Phytochemicals
Acta cir. bras ; 33(12): 1061-1066, Dec. 2018. tab
Article in English | LILACS | ID: biblio-973491


Abstract Purpose: To investigate the role of atenolol in the gene expression of caspase 1 (Casp1) and Bcl2L1 on vascular endothelium of rat intestine after ischemia and reperfusion (IR). Methods: Eighteen adult male Wistar rats were randomly divided into 3 groups (n=6): SG (Sham group): no clamping of the superior mesenteric artery; IRG: IR plus saline group: IRG+At: IR plus Atenolol group. Rats from IRG and IRG+At were subjected to 60 min of intestinal ischemia and 120 min of reperfusion. Atenolol (2mg/kg) or saline were injected in the femoral vein 5 min before ischemia, 5 min and 55 min after reperfusion. Thereafter, intestinal segments were appropriately removed and processed for Endothelial Cell Biology Rat RT2 Profiler PCR Array. Results: the anti-apoptotic Bcl2L1 gene expression was significantly down-regulated (-1.10) in the IRG and significantly up-regulated in the IRG+At (+14.15). Meanwhile, despite Casp1 gene expression was upregulated in both groups, it was significantly higher in the IRG (+35.06) than the IRG+At (+6.68). Conclusions: Atenolol presents antiapoptotic effects on rat intestine subjected to IR partly by the up-regulation of the anti-apoptotic Bcl2L1 gene expression. Moreover, atenolol can mitigate the pro-apoptotic and pro-inflammatory effects of Casp1 gene on rat intestine after IR.

Animals , Male , Atenolol/pharmacology , Reperfusion Injury/prevention & control , Gene Expression/drug effects , Protective Agents/pharmacology , Caspase 1/drug effects , bcl-X Protein/drug effects , Intestine, Small/blood supply , Time Factors , Endothelium, Vascular , Random Allocation , Down-Regulation/drug effects , Up-Regulation/drug effects , Polymerase Chain Reaction , Reproducibility of Results , Treatment Outcome , Rats, Wistar , Mesenteric Artery, Superior , Apoptosis/drug effects , Constriction , Cytoprotection/drug effects , Caspase 1/genetics , bcl-X Protein/genetics , Mesenteric Ischemia/prevention & control
Acta cir. bras ; 33(11): 983-990, Nov. 2018. graf
Article in English | LILACS | ID: biblio-973479


Abstract Purpose: To investigate the efficacy and mechanisms of root tuber of Polygonum ciliinerve (Nakai) ohwi (rPC) which has been used to treat bacterial infection in traditional Chinese medicine. Methods: With the mouse model of Staphylococcus aureus (S. aureus) pneumonia, the phenotype of rPC treated mice, including body weight, mortality, lung slices and bacterial burden were evaluated. Furthermore, inflammatory factors in bronchoalveolar lavage (BAL) were determined by ELISA and the distribution of T cells in lung was assessed by immunofluorescence assay. Results: rPC treatment could dose-dependently reduce weight loss and mortality in S. aureus-infected mice. Upon 10 mg/ml rPC treatment, S. aureus-infected mice showed about 8 grams increase in body weight (P<0.001) and 50% enhancement in mortality. The integrity of lung tissue and bacterial burden were also improved by rPC treatment. Moreover, rPC was found to modulate the immune response in infection. Conclusion: rPC has therapeutic potential for S. aureus infections and pneumonia with immunomodulatory functions.

Animals , Pneumonia, Staphylococcal/prevention & control , Staphylococcus aureus/drug effects , Drugs, Chinese Herbal/pharmacology , Protective Agents/pharmacology , Polygonum/chemistry , Immunomodulation/drug effects , Anti-Bacterial Agents/pharmacology , Pneumonia, Staphylococcal/pathology , Pneumonia, Staphylococcal/drug therapy , Time Factors , Enzyme-Linked Immunosorbent Assay , Bronchoalveolar Lavage Fluid/chemistry , Immunohistochemistry , Colony Count, Microbial , Reproducibility of Results , Interleukin-6/analysis , Tumor Necrosis Factor-alpha/analysis , Treatment Outcome , Chemokine CCL2/analysis , Lung/drug effects , Lung/pathology , Mice, Inbred C57BL
Arq. bras. oftalmol ; 81(6): 505-509, Nov.-Dec. 2018. tab, graf
Article in English | LILACS | ID: biblio-973848


ABSTRACT Purpose: This study aimed to compare the effectiveness of eye drops containing a combination of sodium hyaluronate and trehalose and sodium hyaluronate for the treatment of corneal cross-linking and epithelial healing. Methods: This study included 46 eyes of 23 keratoconus patients who underwent corneal cross-linking on both eyes. Unpreserved trehalose 30 mg/mL and sodium hyaluronate 1.5 mg/mL (Thealoz Duo®; Thea, France) were applied six times a day on one eye of each patient and unpreserved sodium hyaluronate 0.15% (Eye Still®; Teka, Inc., Istanbul) was applied on the other eye. Patients were examined daily until complete re-epithelialization. Postoperative examinations to assess the measured size of epithelial defect were performed using slit-lamp biomicroscopy. Results: The study included 23 patients (13 females and 10 males) with a mean age of 20.9 ± 10.3 years. Corneal epithelial healing time after cross-linking was 2.3 ± 1.2 days for the trehalose and sodium hyaluronate group and 3.8 ± 2.9 days for the sodium hyaluronate group (p=0.03). Conclusion: The application of eye drops containing the combination of trehalose and sodium hyaluronate resulted in faster corneal re-epithelialization following corneal cross-linking than that of eye drops containing sodium hyaluronate alone.

RESUMO Objetivo: Este estudo teve como objetivo comparar a eficácia de colírios contendo uma combinação de hialurônico de sódio e hialuronato de sódio e trealose para o tratamento da cicatrização epitelial em pacientes com cross-linking corneano. Métodos: Este estudo inclui 46 olhos de 23 pacientes com ceratocone, que foram operados com cross-linking corneano em ambos os olhos. Trealose não preservada 30 mg/mL e hialuronato de sódio 1,5 mg/mL (Thealoz Duo®; Thea, França) foram aplicados seis vezes por dia em um olho de cada paciente e hialuronato de sódio não conservado, 0,15% (Eye Still®; Teka, Inc., Istambul) foi aplicada no outro olho. Os pacientes foram examinados diariamente até a completa reepitelização. Exames pós-operatórios para avaliar o tamanho medido do defeito epitelial foram realizados usando biomicroscopia com lâmpada de fenda. Resultados: O estudo incluiu 23 pacientes (13 mulheres e 10 homens) com idade média de 20,9 ± 10,3. O tempo de cicatrização epitelial da córnea após o cross-linking foi de 2,3 ± 1,2 dias para o grupo trealose e hialuronato de sódio e 3,8 ± 2,9 dias para o grupo hialurônico de sódio (p=0,03). Conclusão: A aplicação de gotas para os olhos contendo combinação de trealose e hialuronato de sódio resultou em uma re-epitelização da córnea mais rápida após o cross-linking corneano do que a de gotas contendo hialurônico de sódio apenas.

Humans , Male , Female , Adult , Young Adult , Trehalose/pharmacology , Wound Healing/drug effects , Epithelium, Corneal/drug effects , Protective Agents/pharmacology , Re-Epithelialization/drug effects , Ophthalmic Solutions/pharmacology , Postoperative Care , Treatment Outcome , Epithelium, Corneal/pathology , Cross-Linking Reagents , Drug Therapy, Combination , Hyaluronic Acid/pharmacology , Keratoconus/surgery
Arq. bras. cardiol ; 111(4): 562-568, Oct. 2018. tab, graf
Article in English | LILACS | ID: biblio-973770


Abstract Background: Restenosis after percutaneous coronary intervention in coronary heart disease remains an unsolved problem. Clusterin (CLU) (or Apolipoprotein [Apo] J) levels have been reported to be elevated during the progression of postangioplasty restenosis and atherosclerosis. However, its role in neointimal hyperplasia is still controversial. Objective: To elucidate the role Apo J in neointimal hyperplasia in a rat carotid artery model in vivo with or without rosuvastatin administration. Methods: Male Wistar rats were randomly divided into three groups: the control group (n = 20), the model group (n = 20) and the statin intervention group (n = 32). The rats in the intervention group were given 10mg /kg dose of rosuvastatin. A 2F Fogarty catheter was introduced to induce vascular injury. Neointima formation was analyzed 1, 2, 3 and 4 weeks after balloon injury. The level of Apo J was measured by real-time PCR, immunohistochemistry and western blotting. Results: Intimal/medial area ratio (intimal/medial, I/M) was increased after balloon-injury and reached the maximum value at 4weeks in the model group; I/M was slightly increased at 2 weeks and stopped increasing after rosuvastatin administration. The mRNA and protein levels of Apo J in carotid arteries were significantly upregulated after rosuvastatin administration as compared with the model group, and reached maximum values at 2 weeks, which was earlier than in the model group (3 weeks). Conclusion: Apo J served as an acute phase reactant after balloon injury in rat carotid arteries. Rosuvastatin may reduce the neointima formation through up-regulation of Apo J. Our results suggest that Apo J exerts a protective role in the restenosis after balloon-injury in rats.

Resumo Fundamento: A reestenose após intervenção coronária percutânea (ICP) após doença coronariana continua um problema não solucionado. Estudos relataram que os níveis de clusterina (CLU), também chamada de apolipoproteína (Apo) J, encontram-se elevados na progressão da reestenose pós-angioplastia e na aterosclerose. Contudo, seu papel na hihperplasia neointimal ainda é controverso. Objetivo: Elucidar o papel da Apo J na hiperplasia neointimal na artéria carótida utilizando um modelo experimental com ratos in vivo, com e sem intervenção com rosuvastatina. Métodos: ratos Wistar machos foram divididos aleatoriamente em três grupos - grupo controle (n = 20), grupo modelo (n = 20), e grupo intervenção com estatina (n = 32). Os ratos no grupo intervenção receberam 10 mg/kg de rosuvastatina. Um cateter Fogarty 2 F foi introduzido para induzir lesão vascular. A formação de neoíntima foi analisada 1, 2, 3 e 4 semanas após lesão com balão. Concentrações de Apo J foram medidas por PCR em tempo real, imuno-histoquímica e western blotting. Resultados: A razão área íntima/média (I/M) aumentou após a lesão com balão e atingiu o valor máximo 4 semanas pós-lesão no grupo modelo; observou-se um pequeno aumento na I/M na semana 2, que cessou após a administração de rosuvastatina. Os níveis de mRNA e proteína da Apo J nas artérias carótidas aumentaram significativamente após administração de rosuvastatina em comparação ao grupo modelo, atingindo o máximo na semana 2, mais cedo em comparação ao grupo modelo (semana 3). Conclusão: A Apo J atuou como reagente de fase aguda após lesão com balão nas artérias carótidas de ratos. A rosuvastatina pode reduzir a formação de neoíntoma por aumento de Apo J. Nossos resultados sugerem que a Apo J exerce um papel protetor na reestenose após lesão com balão em ratos.

Animals , Male , Angioplasty, Balloon, Coronary/adverse effects , Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology , Carotid Artery Injuries/drug therapy , Coronary Restenosis/drug therapy , Clusterin/drug effects , Anticholesteremic Agents/pharmacology , Time Factors , Enzyme-Linked Immunosorbent Assay , Immunohistochemistry , Carotid Arteries/drug effects , Carotid Arteries/pathology , Random Allocation , Blotting, Western , Reproducibility of Results , Treatment Outcome , Tunica Media/drug effects , Tunica Media/pathology , Tunica Intima/drug effects , Tunica Intima/pathology , Rats, Wistar , Protective Agents/pharmacology , Carotid Artery Injuries/etiology , Carotid Artery Injuries/pathology , Coronary Restenosis/etiology , Coronary Restenosis/pathology , Clusterin/analysis , Real-Time Polymerase Chain Reaction , Rosuvastatin Calcium/pharmacology
Rev. bras. cir. cardiovasc ; 33(4): 384-390, July-Aug. 2018. tab, graf
Article in English | LILACS | ID: biblio-958430


Abstract Objective: This study aimed to investigate the protective effects of baicalin on myocardial infarction in rats and explore the related mechanisms. Methods: Fifty Sprague Dawley rats were randomly divided into the control, model, and low-, medium- and high-dose baicalin groups. The latter 3 groups were intraperitoneally injected with baicalin, with a dose of 12.5, 25 and 50 mg/kg, respectively. Then, the myocardial infarction model was established. The hemodynamic of rats was tested, the serum lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), prostacyclin (PGI2) and thromboxane A2 (TXA2) were determined, the myocardial superoxide dismutase (SOD) and malondialdehyde (MDA) levels were detected, and the myocardial B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X (Bax) protein expressions were determined. Results: Compared with the model group, in the high-dose baicalin group the ST segment height and LVEDP were significantly decreased (P<0.05), the LVSP was significantly increased (P<0.05), the serum LDH, CK-MB and TXA2 levels were significantly decreased (P<0.05), the PGI2 level was significantly increased (P<0.05), the myocardial SOD level was significantly increased (P<0.05), and the myocardial MDA level was significantly decreased (P<0.05); the myocardial Bcl-2 protein level was significantly increased, and the Bax protein level was significantly decreased (P<0.05). Conclusion: Baicalin has protective effects on myocardial infarction in rats. The possible mechanisms may be related to its resistance to oxidative stress, and up-regulation of Bcl-2 protein expression and down-regulation of Bax protein expression in myocardial tissue.

Animals , Flavonoids/pharmacology , Protective Agents/pharmacology , Myocardial Infarction/prevention & control , Reference Values , Superoxide Dismutase/analysis , Thromboxane A2/blood , Enzyme-Linked Immunosorbent Assay , Random Allocation , Reproducibility of Results , Chromatography, High Pressure Liquid , Epoprostenol/blood , Treatment Outcome , Rats, Sprague-Dawley , Genes, bcl-2 , Creatine Kinase, MB Form/blood , bcl-2-Associated X Protein/analysis , Hemodynamics/drug effects , L-Lactate Dehydrogenase/blood , Malondialdehyde/analysis
Int. braz. j. urol ; 44(3): 617-622, May-June 2018. graf
Article in English | LILACS | ID: biblio-954058


ABSTRACT Objective: To investigate the effect of papaverine and alprostadil on testicular torsion-detorsion injury in rats. Materials and Methods: A total of 40 male Wistar-Albino rats were used in this study. Four hours of right testicular torsion was applied to each group, excluding sham oper- ated group. The torsion-detorsion (T/D), T/D + papaverine and T/D + alprostadil groups received saline, papaverine and alprostadil at the same time as surgical detorsion, respectively. At 14 days after the surgical detorsion, ischaemic changes and the degree of damage were evaluated with Cosentino scoring and the Johnson tubular biopsy score (JTBS). Results: JTBS was determined as 8.8±2.7 in the Sham group, 5.08±1.9 in the T/D+papaverine group, 5.29±2.3 in the T/D +alprostadil group and 2.86±1.9 in the TD group. The JTBS was determined to be statistically significantly high in both the T/D + papaverine group and the T/D + alprostadil group compared to the T/D group (p=0.01, p=0.009). In the T/D + papaverine group, 3 (43%) testes were classified as Cosentino 2, 3 (43%) as Cosentino 3 and 1 (14%) as Cosentino 4. In the T/D +alprostadil group, 5 (50 %) testes were classified as Cosentino 2, 3 (30 %) as Cosentino 3 and 2 (20%) as Cosentino 4. Conclusion: The present study indicated that spermatic cord administration of alprostadil and papaverine showed a protective effect against ischemia/reperfusion injury after right-side testes torsion and histological changes were decreased after testicular ischemia reperfusion injury.

Animals , Male , Papaverine/therapeutic use , Spermatic Cord Torsion/prevention & control , Testis/blood supply , Vasodilator Agents/pharmacology , Alprostadil/pharmacology , Ischemia/prevention & control , Papaverine/pharmacology , Spermatic Cord Torsion/pathology , Testis/pathology , Vasodilator Agents/therapeutic use , Biopsy , Severity of Illness Index , Alprostadil/therapeutic use , Reperfusion Injury/prevention & control , Random Allocation , Reproducibility of Results , Treatment Outcome , Rats, Wistar , Protective Agents/therapeutic use , Protective Agents/pharmacology
Arq. gastroenterol ; 55(2): 138-141, Apr.-June 2018. tab
Article in English | LILACS | ID: biblio-950505


ABSTRACT BACKGROUND: Extracts obtained from plants and fruits provide a relatively safe and practical alternative for the conventional medicine of gastrointestinal diseases. The specie Eugenia mattosii, popularly known in Brazil as "cerejinha", belongs to Myrtaceae family. Species of this family present pharmacological properties, and can be used in the treatment of gastrointestinal disorders. OBJECTIVE: The aim of this study was to determine the phytochemical profile and evaluate the gastroprotective activity of Eugenia mattosii fruits. METHODS: Phytochemical analysis was carried out by thin layer chromatography and gastroprotective assays were performed using two experimental models: acute ulcer model induced by ethanol/HCl and acute ulcer model induced by non-steroidal anti-inflammatory drug (indomethacin). Total lesion area (mm2) and relative lesion area (%) were determined. RESULTS: The results of the phytochemical analysis indicated that the bark and pulp and seeds of E. mattosii present phenolic compounds, terpenes and/or steroids. In gastric ulcer model induced by ethanol was evidenced significant reduction of damaged areas for doses of 50 and 250 mg/ kg of seeds methanol extract, while in the indomethacin-induced ulcer model, all parts of the fruit presented defense capability of the gastric mucosa by reducing lesions at doses of 50, 125 and 250 mg/kg. CONCLUSION: The results demonstrate that the specie E. mattosii has bioactive compounds that provide gastroprotective activity, presenting possible therapeutic potential.

RESUMO CONTEXTO: Extratos obtidos de plantas e frutos fornecem uma alternativa relativamente segura e prática para os remédios convencionais de doenças gastrointestinais. A espécie Eugenia mattosii, popularmente conhecida no Brasil como "cerejinha", pertence à família Myrtaceae. Espécies desta família apresentam propriedades farmacológicas e podem ser utilizadas no tratamento de distúrbios gastrointestinais. OBJETIVO: O objetivo deste estudo foi determinar o perfil fitoquímico e avaliar a atividade gastroprotetora dos frutos de Eugenia mattosii. MÉTODOS: A análise fitoquímica foi realizada por cromatografia em camada delgada e dois modelos experimentais foram utilizados para avaliação da atividade gastroprotetora em camundongos: modelo de úlcera gástrica induzida por anti-inflamatório não-esteroidal (indometacina) e modelo de úlcera gástrica induzida por etanol/HCl. RESULTADOS: Os resultados da análise fitoquímica indicaram que a casca e polpa e as sementes de E. mattosii apresentam compostos fenólicos, terpenos e/ou esteroides. No modelo de úlcera gástrica induzido pelo etanol, foi evidenciada redução significativa de áreas danificadas para doses de 50 e 250 mg/kg do extrato das sementes, enquanto no modelo de úlcera induzida por indometacina, todas as partes do fruto apresentaram capacidade de defesa da mucosa gástrica ao reduzir as lesões nas doses de 50, 125 e 250 mg/kg. CONCLUSÃO: Os resultados demonstram que a espécie E. mattosii possui compostos bioativos com atividade gastroprotetora, apresentando possível potencial terapêutico.

Animals , Female , Mice , Stomach Ulcer/prevention & control , Plant Extracts/pharmacology , Protective Agents/pharmacology , Eugenia/chemistry , Fruit/chemistry , Gastric Mucosa/drug effects , Anti-Ulcer Agents/pharmacology , Seeds/chemistry , Stomach Ulcer/chemically induced , Brazil , Plant Extracts/administration & dosage , Indomethacin , Disease Models, Animal , Ethanol , Phytochemicals/pharmacology , Phytotherapy , Anti-Ulcer Agents/administration & dosage , Antioxidants/analysis , Antioxidants/pharmacology
Acta cir. bras ; 33(4): 362-374, Apr. 2018. tab, graf
Article in English | LILACS | ID: biblio-886283


Abstract Purpose: To investigate the prophylactic and therapeutical effects of sildenafil in a model of acute radiation proctitis (ARP). Methods: All experimental procedures of this study was examined by histopathological, immunohistochemical and transmission electron microscopic analysis. Results: Our histopathological evaluations indicated significant increases in lesion severity, cryptic apsis, cryptitis, cryptic distortion, reactive atypia and infiltration depth of the control (proctitis) group. While the prophylaxis group and the treatment group had significantly lower scores. High-dose group showed similar results as prophylaxis group. Histopathological findings of the prophylaxis group was more significant than the treatment group. Immunoreactivities of IL-1β, FGF-2, TNF- α and HIF-1α increased in the control group especially in the epithelial and cryptic regions. On the contrary, sildenafil application caused significant decreases of inflammatory markers in all treatment groups, specifically better results in the prophylaxis group. Conclusion: The sildenafil has anti-inflammatory effects on ARP, as well as protective effects against ARP and the protective effect of sildenafil surpasses its therapeutic effect histopathologically.

Animals , Proctitis/etiology , Proctitis/drug therapy , Radiation Injuries, Experimental/drug therapy , Post-Exposure Prophylaxis/methods , Sildenafil Citrate/pharmacology , Anti-Inflammatory Agents/pharmacology , Proctitis/pathology , Radiation Injuries, Experimental/pathology , Rectum/pathology , Time Factors , Severity of Illness Index , Immunohistochemistry , Random Allocation , Reproducibility of Results , Fibroblast Growth Factor 2/analysis , Tumor Necrosis Factor-alpha/analysis , Treatment Outcome , Protective Agents/pharmacology , Vascular Endothelial Growth Factor A/analysis , Microscopy, Electron, Transmission , Hypoxia-Inducible Factor 1, alpha Subunit/analysis , Interleukin-1beta/analysis
Acta cir. bras ; 33(3): 207-215, Mar. 2018. tab, graf
Article in English | LILACS | ID: biblio-886274


Abstract Purpose: To investigate whether oxymatrine (OMT) prevents hepatic fibrosis in rats by regulating liver transforming growth factor β1 (TGF-β1) level. Methods: Hepatic fibrosis was induced in rats by thioacetamide (TAA). Blood was collected at the end of week 12 to determine the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and glutathione (GSH). Changes in liver tissue were observed after hematoxylin-eosin (HE) staining. Results: Fibrosis was confirmed by Masson's collagen staining. Liver TGF-β1 level was determined by ELISA. OMT significantly reduced serum ALT and AST but increased GSH levels in rats with hepatic fibrosis. Moreover, it significantly improved liver histology in rats with TAA-induced hepatic fibrosis. It significantly decreased liver TGF-β1 level compared to that in the untreated group. It also significantly reduced collagen deposition in rats. Conclusion: Oxymatrine is effective in protecting rats from thioacetamide-induced hepatic fibrosis by regulating TGF-β1 expression.

Animals , Male , Rats , Quinolizines/pharmacology , Protective Agents/pharmacology , Alkaloids/pharmacology , Transforming Growth Factor beta1/metabolism , Liver Cirrhosis, Experimental/prevention & control , Aspartate Aminotransferases/blood , Rats, Sprague-Dawley , Transforming Growth Factor beta1/drug effects , Liver Cirrhosis, Experimental/chemically induced , Liver Cirrhosis, Experimental/metabolism
An. acad. bras. ciênc ; 90(1): 267-281, Mar. 2018. tab, graf
Article in English | LILACS | ID: biblio-886889


ABSTRACT Dyslipidemias are associated with the incidence of cardiovascular diseases, obesity, diabetes, hypertension and hepatic steatosis, being the cause of morbidity and mortality. This study investigated the effects of lychee peel flour (PF) on serum levels of total cholesterol (TC), low-density lipoprotein (LDL-c), triacylglycerols (TAG) and various parameters related to obesity, in rats fed a hypercholesterolemic diet. Therefore, 20 male rats were used. In the first 21 days, the animals were fed a hypercholesterolemic diet, except for control group. In the following 21 days, their diets were modified, and they received a standard diet (Control); hypercholesterolemic (Hyper); hypercholesterolemic + 5% PF (PF5) and hypercholesterolemic + 10% PF (PF10). The results revealed that PF intake attenuated weight gain, reduced body mass index, glucose and the levels of TAG, TC, LDL-c, hepatic enzymes and leptin, besides the percentage of hepatic lipids, liver lipid peroxidation and frequency of severe steatosis. Histological studies of the aorta did not show the formation of the atheromatous plaque. These results reinforce its potential to reduce the risk of diseases associated with obesity.

Animals , Male , Litchi/chemistry , Fatty Liver/prevention & control , Diet, High-Fat , Hypercholesterolemia/prevention & control , Liver/drug effects , Aspartate Aminotransferases/blood , Lipid Peroxidation , Cholesterol/blood , Rats, Wistar , Protective Agents/pharmacology , Alanine Transaminase/blood , Fatty Liver/diet therapy , Fatty Liver/blood , Hypercholesterolemia/diet therapy , Hypercholesterolemia/blood , Lipoproteins, LDL/blood