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1.
Electron. j. biotechnol ; 52: 13-20, July. 2021. tab, graf, ilus
Article in English | LILACS | ID: biblio-1283173

ABSTRACT

BACKGROUND: In fish farming, the plant extracts containing antioxidant compounds have been added to the diet for enhancing pathogen resistance. In vitro studies evaluating the antioxidant effect of herbal extracts on fish cell models have focused on ROS production and the respiratory burst mechanism. However, the effects on enzymatic antioxidant defense on salmon leukocytes have not been evaluated. This study aims to evaluate the enzymatic antioxidant defense and ROS-induced cell damage in Salmon Head Kidney-1 (SHK-1) cell line exposed to polyphenol-enriched extract from Sambucus nigra flowers. RESULTS: Firstly, the Total Reactive Antioxidant Power (TRAP) assay of elderflower polyphenol (EP) was evaluated, showing 459 and 489 times more active than gallic acid and butyl hydroxy toluene (BHT), respectively. The toxic effect of EP on salmon cells was not significant at concentrations below 120 mg/ mL and no hemolysis activity was observed between 20 and 400 mg/mL. The treatment of SHK-1 cell line with EP decreased both the lipid peroxidation and protein oxidation induced by H2O2, which could be associated with decreasing oxidative stress in the SHK-1 cells since the GSH/GSSG ratio increased when only EP was added. CONCLUSIONS: These results suggest that plant extracts enriched with polyphenols could improve the enzymatic antioxidant defense of salmon leukocytes and protect the cells against ROS-induced cell damage


Subject(s)
Salmon , Plant Extracts/pharmacology , Sambucus nigra/chemistry , Polyphenols/pharmacology , Lipid Peroxidation , Free Radical Scavengers , Reactive Oxygen Species , Aquaculture , Oxidative Stress , Salmo salar , Disease Resistance , Leukocytes , Antioxidants
2.
Electron. j. biotechnol ; 45: 46-52, May 15, 2020. tab, graf, ilus
Article in English | LILACS | ID: biblio-1177424

ABSTRACT

BACKGROUND: The present study analyzed the synergistic protective effect of ß-alanine and taurine against myocardial ischemia/reperfusion. Myocardial infarct size, lipid peroxidation, and levels of glutathione peroxidase (Gpx), superoxide dismutase (SOD), reduced glutathione (GSH), catalase, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), reactive oxygen species (ROS), apoptosis, and the mRNA and protein expression of Janus kinase 2 (JAK2) and signal transducer and activator 3 of transcription (STAT3) were determined. The molecular docking was carried out by using AutoDock 4.2.1. RESULTS: Combined treatment with ß-alanine and taurine reduced myocardial infarct size, lipid peroxidation, inflammatory marker, ROS levels, and apoptosis and increased Gpx, SOD activity, GSH, and catalase activity. Furthermore, combined treatment significantly reduced JAK2 and STAT3 mRNA and protein expression compared with the control. The small molecule was docked over the SH2 domain of a STAT3, and binding mode was determined to investigate the inhibitory potential of ß-alanine and taurine. ß-Alanine bound to SH2 domain with ΔG of -7.34 kcal/mol and KI of 1.91 µM. Taurine bound to SH2 domain with ΔG of -7.38 kcal/mol and KI of 1.95 µM. CONCLUSION: Taken together, these results suggest that the combined supplementation of ß-alanine and taurine should be further investigated as an effective therapeutic approach in achieving cardioprotection in myocardial ischemia/reperfusion.


Subject(s)
Animals , Male , Rats , Taurine/therapeutic use , Cardiotonic Agents/therapeutic use , Reperfusion Injury/drug therapy , beta-Alanine/therapeutic use , Myocardial Ischemia/drug therapy , Superoxide Dismutase , Immunohistochemistry , Lipid Peroxidation , Reactive Oxygen Species , Rats, Wistar , Reverse Transcriptase Polymerase Chain Reaction , Disease Models, Animal , Janus Kinase 2 , Molecular Docking Simulation , Glutathione Peroxidase , Heart Diseases/drug therapy , Inflammation
3.
Braz. j. med. biol. res ; 53(6): e9237, 2020. tab, graf
Article in English | LILACS, ColecionaSUS | ID: biblio-1132520

ABSTRACT

We investigated changes in oxidative biomarkers in brain regions such as brainstem, cerebellum, and cerebral cortex of 3-, 6-, 18-, 24-, and 30-month-old rats. We also assessed the effects of low-intensity exercise on these biomarkers in these regions of 6-, 18-, and 24-month-old rats that started exercise on a treadmill at 3, 15, and 21 months of age, respectively. Radiographic images of the femur were taken for all rats. A total of 25 rats (age: twelve 6-, ten 18-, ten 24-, and three 30-month-old rats) were used. Lipid hydroperoxide levels increased in cerebellum at 18 months. Total antioxidant activity exhibited lowest values in brainstem at 3 months. Superoxide dismutase activity did not exhibit significant changes during aging. Total thiol content exhibited lowest values in brain regions of 24- and 30-month-old rats. Exercise reduced total thiol content in brainstem at 6 months, but no change occurred in other regions and other ages. Femur increased its length and width and cortical thickness with advancing age. No change occurred in medullary width. Radiolucency increased and sclerosis was found in cortical and medullary bone with advancing age. Exercise reduced radiolucency and medullary sclerosis. Therefore, aging differentially changed oxidative biomarkers in different brain regions and radiographic measures of the femur. Low-intensity exercise only ameliorated some radiographic measurements of femur. Since the present study possessed limitations (small number of rats per group), a beneficial effect of regular low-intensity exercise on oxidative markers in brain cannot be ruled out.


Subject(s)
Animals , Male , Rats , Physical Conditioning, Animal/physiology , Brain/metabolism , Aging/physiology , Oxidative Stress/physiology , Femur/diagnostic imaging , Lipid Peroxides/analysis , Oxidation-Reduction , Aging/metabolism , Biomarkers/analysis , Lipid Peroxidation , Rats, Wistar , Femur/chemistry
4.
Acta Physiologica Sinica ; (6): 566-574, 2020.
Article in Chinese | WPRIM | ID: wpr-878202

ABSTRACT

Ferroptosis is a newly discovered non-apoptotic form of regulated cell death driven by iron-dependent lipid peroxidation. The present studies have shown that many metabolic processes and homeostasis are affected by ferroptosis. It is related to many lung diseases, including acute lung injury, chronic obstructive pulmonary disease and pulmonary fibrosis, etc. Currently, the research on ferroptosis is still in its infancy. Previous studies have confirmed that ferroptosis is regulated by a variety of genes, and the mechanism is complex, mainly involving iron homeostasis and lipid peroxidation metabolism. This review summarizes some regulation networks of metabolic processes associated with ferroptosis and discusses the roles of ferroptosis in the pathophysiological progression of many lung diseases. We expected to provide new ideas and references for the treatment of these diseases.


Subject(s)
Ferroptosis , Humans , Iron , Lipid Peroxidation , Metabolic Networks and Pathways , Pulmonary Disease, Chronic Obstructive
5.
Rev. Nutr. (Online) ; 33: e190097, 2020. tab, graf
Article in English | LILACS | ID: biblio-1101407

ABSTRACT

ABSTRACT Objective The purpose of this study is to determine the phenolic and flavonoid contents, and antioxidant activities and neuroprotective effects of powdered coffee sample of a commercial coffee brand originated from Sivas, Turkey. Methods Total phenolic, flavonoid and antioxidant contents, enzymatic and non-enzymatic antioxidative activities based on 2,2-diphenyl-1-picrylhydrazyl free radical scavenging activity, metal chelating potential, reducing power, superoxide dismutase and catalase activity tests and lipid peroxidation inhibition potentials of the ethanolic and aqueous extracts of the coffee sample were assayed using the commonly preferred spectrophotometric methods. Furthermore the extracts' cholinesterase and tyrosinase inhibition potentials were evaluated. Phenolic profiles of the coffee sample were investigated using high performance liquid chromatography. Results Catechin was the most frequently detected phenolic acid. In addition, it was demonstrated that the water extract has a significant impact when compared with standard antioxidants. While the SC50 (sufficient concentration to obtain 50% of a maximum scavenging capacity) value for the scavenging activity of 2,2-diphenyl-1-picrylhydrazyl free radical was calculated as being 0.08mg/mL for water extract, the amount of chelating agents with half Fe2+ ions in the medium was found to be 0.271mg/mL. Additionally, it was shown that 0.1mg/mL concentration of both extracts prevents lipid peroxidation by 8%. Compared with standard drugs, inhibition potentials of cholinesterase and tyrosinase enzymes were considered as moderately acceptable in these samples. Conclusion Besides the extracts' enzymatic antioxidant activity, their inhibition potential on cholinesterase and tyrosinase enzymes - which are important clinical enzymes - reveal that this natural source can be used as a valuable resource in different fields, especially in medicine.


RESUMO Objetivo O objetivo deste estudo é determinar o conteúdo fenólico e flavonoide, bem como as atividades antioxidantes e os efeitos neuroprotetores de uma amostra de café em pó de uma promissora marca comercial proveniente de Sivas, Turquia. Métodos A partir dos métodos espectrofotométricos comumente utilizados, foram analisados os seguintes aspectos da amostra de café: teores de fenólicos totais, flavonoides e antioxidantes; atividades antioxidantes enzimáticas e não enzimáticas, baseadas na atividade de eliminação de radicais livres de 2,2-difenil-1-picrilhidrazila potencial quelante de metais; poder redutor; testes de atividade de superóxido dismutase e catalase; e potenciais de inibição da peroxidação lipídica dos extratos etanólicos e aquosos. Além disso, foram avaliados os potenciais de inibição da colinesterase e da tirosinase dos extratos. Os perfis fenólicos da amostra de café foram investigados por cromatografia líquida de alta eficiência. Resultados Entre os ácidos fenólicos estudados, o mais detectado foi a catequina. Especialmente, foi demonstrado que o extrato de água tem um impacto significativo quando comparado com os antioxidantes padrão. Determinou--se que o valor de SC50 (a concentração suficiente para obter 50% da capacidade máxima de eliminação) da atividade de eliminação do radical 2,2-difenil-1-picrilhidrazilab/para extrato de água era de 0,08mg/mL, enquanto a quantidade de agentes quelantes com metade de Fe2+ íons na média foi encontrada como 0,271mg/mL. Também foi demonstrado que a concentração de 0,1mg/mL de ambos os extratos inibe a peroxidação lipídica em cerca de 8%. Comparado com drogas padrão, os potenciais de inibição das amostras nas enzimas e tirosinase foram aceitáveis como moderados. Conclusão Os resultados mostram que, além de terem atividade antioxidante enzimática, os extratos apresentam potencial de inibição das enzimas colinesterase e tirosinase, que são importantes enzimas clínicas, o que revela que essa fonte natural pode ser usada como um recurso valioso em vários campos, principalmente na medicina.


Subject(s)
Cholinesterase Inhibitors , Lipid Peroxidation , Monophenol Monooxygenase , Coffee , Phenolic Compounds , Free Radicals , Antioxidants
6.
Rev. cuba. obstet. ginecol ; 45(4): e496, oct.-dic. 2019. tab, graf
Article in Spanish | LILACS, CUMED | ID: biblio-1126710

ABSTRACT

RESUMEN Introducción: La preeclampsia es uno de los síndromes en mujeres embarazadas que afecta al menos 3 - 8 por ciento de todos los embarazos. Objetivo: Desarrollar un modelo predictivo de preeclampsia a partir del estado redox en embarazadas, que clasifique a las mujeres pertenecientes a los grupos de gestantes preeclámpticas y gestantes sanas. Métodos: Se realizó un estudio analítico transversal. Los parámetros bioquímicos y clínicos se evaluaron utilizando el análisis de componentes principales para identificar las variables más influyentes en la aparición de preeclampsia. Los seleccionados como las variables más importantes fueron evaluados por el análisis discriminante lineal de Fisher. Resultados: El análisis de componentes principales determinó la varianza del set de datos, mostrando la relación con los procesos de peroxidación lipídica, metabolismo de proteínas, daño a tejidos y microangiopático, considerados factores en la fisiopatología de la preeclampsia. Las variables más influyentes fueron usadas para modelar una función discriminante capaz de clasificar gestantes sanas y preeclámpticas. El valor de Lambda de Wilks y el alto autovalor asociado a la función discriminante muestran el poder discriminante del modelo. La ecuación obtenida fue validada con el método Leave one out y reveló un excelente poder clasificatorio del mismo. Conclusiones: El modelo predictivo puede ser considerado como apropiado para clasificar los casos de preeclampsia, y muestran a los biomarcadores como buenos candidatos para la clasificación y como potenciales indicadores predictivos de preeclampsia(AU)


ABSTRACT Introduction: Preeclampsia is one of the syndromes in pregnant women that affects at least 3 - 8 percent of all pregnancies. Objective: To develop a predictive model of preeclampsia from the redox state in pregnant women, which allows to classify them in groups of preeclamptic pregnant women and healthy pregnant women. Methods: A cross-sectional analytical study was performed. Biochemical and clinical parameters were evaluated using principal component analysis to identify the most influential variables in the occurrence of preeclampsia. Those selected as the most important variables were evaluated by Fisher's linear discriminant analysis. Results: The main component analysis determined the variance of the data set, showing the relationship with lipid peroxidation processes, protein metabolism, tissue damage and microangiopathy, considered factors in the pathophysiology of preeclampsia. The most influential variables were used to model a discriminant function capable of classifying healthy and preeclamptic pregnant women. Wilks Lambda value and the high eigenvalue associated with the discriminant function show the discriminant power of the model. The equation obtained was validated with the Leave one out method and revealed excellent classifying power. Conclusions: The predictive model can be considered as appropriate to classify pre-eclampsia cases, and to show biomarkers as good candidates for classification and as potential predictive indicators of pre-eclampsia(AU)


Subject(s)
Humans , Female , Pregnancy , Pre-Eclampsia/diagnosis , Discriminant Analysis , Lipid Peroxidation , Cross-Sectional Studies
7.
Arq. neuropsiquiatr ; 77(12): 881-887, Dec. 2019. tab, graf
Article in English | LILACS | ID: biblio-1055207

ABSTRACT

ABSTRACT Induction of long-term potentiation (LTP) increases the storage capacity of synapses in the hippocampal dentate gyrus (DG). Irisin is a myokine generated from FNDC5 (a gene precursor) during exercise. Although intra-cornu ammonis 1 administration of irisin fortifies LTP in mice with Alzheimer's disease, the effects of intra-DG injection of irisin on the LTP in rats remains to be elucidated in vivo. In this study, male Wistar rats were randomly divided into a control group (saline), irisin (0.5, 1, and 1.5 μg/rat), and dimethyl sulfoxide (DMSO). After treatment, the population spike (PS) amplitude and slope of excitatory postsynaptic potentials (EPSP) were measured in the DG of rats in vivo. Moreover, following completion of the experiments, the stimulating and recording sites in the hippocampus were confirmed histologically from brain sections. Furthermore, biochemical assays like malondialdehyde (MDA), total antioxidant capacity (TAC), and total oxidant status (TOS) were evaluated (the antioxidant markers were analyzed in the plasma). Our results suggest that all doses of irisin (0.5, 1, 1.5 μg/rat) caused an increase in the EPSP slope and PS amplitude when compared with the control group. In addition, the results obtained showed that irisin decreased TOS and MDA levels while increasing TAC levels as a marker of lipid peroxidation in plasma. The present report provides direct evidence that irisin affects the activity-dependent synaptic plasticity in the dentate gyrus.


RESUMO A indução de potenciação de longo prazo (LTP) aumenta a capacidade de armazenamento das sinapses no giro denteado (DG) do hipocampo. A irisina é uma miocina gerada a partir do FNDC5 (um precursor genético) durante o exercício. Embora a administração intra-Cornu Ammonis1 de irisina fortaleça a LTP em camundongos com doença de Alzheimer, os efeitos da injeção intra-denteada de irisina sobre a LTP em ratos ainda precisam ser elucidados in vivo. Neste estudo, ratos Wistar machos foram divididos aleatoriamente em um grupo controle (solução salina), irisina (0,5, 1 e 1,5 μg / rato) e dimetilsulfóxido (DMSO). Após o tratamento, a amplitude do pico populacional (PS) e a variação dos potenciais pós-sinápticos excitatórios (EPSP) foram medidos no DG de ratos in vivo. Além disso, após a conclusão das experiências, os locais de estimulação e registro no hipocampo foram confirmados histologicamente a partir de secções do cérebro. Adicionalmente, ensaios bioquímicos como malondialdeído (MDA), capacidade antioxidante total (TAC) e status oxidante total (TOS) foram avaliados (os marcadores antioxidantes foram analisados no plasma). Nossos resultados sugerem que todas as doses de irisina (0,5, 1, 1,5 μg / rato) causaram um aumento na variação da EPSP e na amplitude da PS quando comparadas com o grupo controle. Além disso, os resultados obtidos mostraram que a irisina diminuiu os níveis de TOS e MDA, enquanto aumentou os níveis de TAC como um marcador da peroxidação lipídica no plasma. O presente estudo fornece evidências diretas de que a irisina afeta a plasticidade sináptica dependente de atividade no DG.


Subject(s)
Animals , Male , Neuropeptides/administration & dosage , Fibronectins/administration & dosage , Long-Term Potentiation/drug effects , Dentate Gyrus/drug effects , Microinjections/methods , Reference Values , Time Factors , Lipid Peroxidation , Random Allocation , Reproducibility of Results , Rats, Wistar , Brain-Derived Neurotrophic Factor/analysis , Brain-Derived Neurotrophic Factor/drug effects , Excitatory Postsynaptic Potentials/drug effects , Malondialdehyde/blood , Antioxidants/analysis
8.
Arq. bras. cardiol ; 113(5): 905-912, Nov. 2019. tab, graf
Article in English | LILACS | ID: biblio-1055041

ABSTRACT

Abstract Background: Arterial hypertension is a precursor to the development of heart and renal failure, furthermore is associated with elevated oxidative markers. Environmental enrichment of rodents increases performance in memory tasks, also appears to exert an antioxidant effect in the hippocampus of normotensive rats. Objectives: Evaluate the effect of environmental enrichment on oxidative stress in the ventrolateral medulla, heart, and kidneys of renovascular hypertensive rats. Methods: Forty male Fischer rats (6 weeks old) were divided into four groups: normotensive standard condition (Sham-St), normotensive enriched environment (Sham-EE), hypertensive standard condition (2K1C-St), and hypertensive enriched environment (2K1C-EE). Animals were kept in enriched or standard cages for four weeks after all animals were euthanized. The level of significance was at p < 0.05. Results: 2K1C-St group presented higher mean arterial pressure (mmHg) 147.0 (122.0; 187.0) compared to Sham-St 101.0 (94.0; 109.0) and Sham-EE 106.0 (90.8; 117.8). Ventrolateral medulla from 2K1C-EE had higher superoxide dismutase (SOD) (49.1 ± 7.9 U/mg ptn) and catalase activity (0.8 ± 0.4 U/mg ptn) compared to SOD (24.1 ± 9.8 U/mg ptn) and catalase activity (0.3 ± 0.1 U/mg ptn) in 2K1C-St. 2K1C-EE presented lower lipid oxidation (0.39 ± 0.06 nmol/mg ptn) than 2K1C-St (0.53 ± 0.22 nmol/mg ptn) in ventrolateral medulla. Furthermore, the kidneys of 2K1C-EE (11.9 ± 2.3 U/mg ptn) animals presented higher superoxide-dismutase activity than those of 2K1C-St animals (9.1 ± 2.3 U/mg ptn). Conclusion: Environmental enrichment induced an antioxidant effect in the ventrolateral medulla and kidneys that contributes to reducing oxidative damage among hypertensive rats.


Resumo Fundamento: A hipertensão arterial é um precursor para o desenvolvimento da insuficiência cardíaca e renal e, além disso, está associada com o aumento dos marcadores oxidativos. O enriquecimento ambiental dos roedores melhora o desempenho em tarefas de memória, e também parece ter um efeito antioxidante sobre o hipocampo dos ratos normotensos. Objetivos: Avaliar o efeito do enriquecimento ambiental sobre o estresse oxidativo no bulbo ventrolateral, coração, e rins de ratos com hipertensão renovascular. Métodos: Quarenta ratos machos, tipo Fischer (6 semanas de idade), foram divididos em quatro grupos: normotensos em condições padrão (Sham-CP), normotensos em ambiente enriquecido (Sham-AE), hipertensos em condições padrão (2R1C-CP), e hipertensos em ambiente enriquecido (2R1C-AE). Os animais foram mantidos em gaiolas enriquecidas ou padrão durante quatro semanas e, por fim, todos os animais foram eutanasiados. O nível de significância foi p < 0,05. Resultados: O grupo 2R1C-CP apresentou pressão arterial média maior (mmHg) 147,0 (122,0; 187,0) quando comparado com os grupos Sham-CP 101,0 (94,0; 109,0) e Sham-AE 106,0 (90,8; 117,8). Observou-se maior atividade das enzimas superóxido dismutase (SOD) (49,1 ± 7,9 U/mg ptn) e da catalase (0,8 ± 0,4 U/mg ptn) no bulbo ventrolateral do grupo 2R1C-AE, em relação à atividade da SOD (24,1 ± 9,8 U/mg ptn) e da catalase (0,3 ± 0,1 U/mg ptn) no grupo 2R1C-CP. No grupo 2R1C-AE, a oxidação lipídica no bulbo ventrolateral foi menor (0,39 ± 0,06 nmol/mg ptn) quando comparado com o grupo 2R1C-CP (0,53 ± 0,22 nmol/mg ptn). Ademais, foi observada maior atividade das enzimas superóxido dismutase nos rins dos animais 2R1C-AE (11,9 ± 2,3 U/mg ptn) em relação aos animais 2R1C-CP (9,1 ± 2,3 U/mg ptn). Conclusão: O enriquecimento ambiental provocou efeito antioxidante no bulbo ventrolateral e nos rins, o que contribuiu para a redução do dano oxidante nos ratos hipertensos.


Subject(s)
Animals , Male , Medulla Oblongata/metabolism , Oxidative Stress , Environment , Housing, Animal , Hypertension, Renovascular/metabolism , Antioxidants/metabolism , Rats, Inbred F344 , Superoxide Dismutase/metabolism , Medulla Oblongata/enzymology , Lipid Peroxidation , Catalase/metabolism , Protein Carbonylation , Arterial Pressure , Heart Ventricles/enzymology , Hypertension, Renovascular/chemically induced , Kidney/enzymology
9.
Arq. bras. cardiol ; 112(5): 545-552, May 2019. tab, graf
Article in English | LILACS | ID: biblio-1011190

ABSTRACT

Abstract Background: Obesity can be characterized by low-grade chronic inflammation and is associated with an excesso production of reactive oxygen species, factors that contribute to coronary heart disease and other cardiomyopathies. Objective: To verify the effects of resistance exercise training on oxidative stress and inflammatory parameters on mice with obesity induced by a high-fat diet (HFD). Methods: 24 Swiss mice were divided into 4 groups: standard diet (SD), SD + resistance exercise (SD + RE), diet-induced obesity (DIO), DIO + RE. The animals were fed SD or HFD for 26 weeks and performed resistance exercises in the last 8 weeks of the study. The insulin tolerance test (ITT) and body weight monitoring were performed to assess the clinical parameters. Oxidative stress and inflammation parameters were evaluated in the cardiac tissue. Data were expressed by mean and standard deviation (p < 0.05). Results: The DIO group had a significant increase in reactive oxygen species levels and lipid peroxidation with reduction after exercise. Superoxide dismutase and the glutathione system showed no significant changes in DIO animals, with an increase in SD + RE. Only catalase activity decreased with both diet and exercise influence. There was an increase in tumor necrosis factor-alpha (TNF-α) in the DIO group, characterizing a possible inflammatory condition, with a decrease when exposed to resistance training (DIO+RE). Conclusion: The DIO resulted in a redox imbalance in cardiac tissue, but the RE was able to modulate these parameters, as well as to control the increase in TNF-α levels.


Resumo Fundamento: A obesidade pode ser caracterizada por uma inflamação crônica de baixo grau e está associada à produção excessiva de espécies reativas de oxigênio, fatores que contribuem para doenças coronarianas e outras cardiomiopatias. Objetivo: Verificar os efeitos do treinamento resistido sobre os parâmetros de estresse oxidativo e parâmetro inflamatório em camundongos com obesidade induzida por dieta hiperlipídica (DIO). Métodos: 24 camundongos Swiss foram divididos em 4 grupos: dieta padrão (DP), DP + exercício resistido (DP+ER), obesidade induzida por DIO, DIO + ER. Os animais foram alimentados por 26 semanas com DP ou hiperlipídica realizando treinamento resistido nas 8 semanas finais do estudo. Para avaliar parâmetros clínicos foi realizado o teste de tolerância à insulina (TTI) e monitoramento do peso corporal. No tecido cardíaco foram avaliados parâmetros de estresse oxidativo e inflamação. Dados expressos por média e desvio padrão (p < 0,05). Resultados: O grupo DIO teve um aumento significativo nos níveis espécies reativas e peroxidação lipídica com redução após o exercício. A superóxido dismutase e o sistema glutationa não demonstraram alterações importantes nos animais DIO, com elevação perante DP+ER. Somente a atividade da catalase reduziu tanto com influência da dieta como do exercício. Ocorreu um aumento do fator de necrose tumoral-alfa (TNF-α) no grupo DIO, caracterizando um possível quadro inflamatório, com redução quando expostos ao treino resistido (DIO+ER). Conclusão: A DIO ocasionou um desequilíbrio redox no tecido cardíaco, porém o ER foi capaz de modular estes parâmetros, bem como controlar o aumento do TNF-α.


Subject(s)
Animals , Male , Rats , Lipid Peroxidation/physiology , Tumor Necrosis Factor-alpha/analysis , Oxidative Stress/physiology , Resistance Training , Diet, High-Fat/adverse effects , Myocardium/chemistry , Physical Conditioning, Animal , Time Factors , Insulin Resistance , Inflammation/physiopathology
10.
Bol. latinoam. Caribe plantas med. aromát ; 18(3): 336-346, mayo 2019. tab, ilus
Article in English | LILACS | ID: biblio-1008047

ABSTRACT

The chemical composition of Mangifera indica L. cv. "Kent" leaves was determined by HPLC-ESI-QTOF-MS/MS. Polyphenolic compounds characterized as benzophenone derivatives were the main components found in extracts (1, maclurin 3-C-(2-O-galloyl)-D- glucoside isomer; 2, maclurin 3-C---D-glucoside; 3, iriflophenone 3-C---D-glucoside; 5, maclurin 3-C-(2,3-di-O-galloyl)---D-glucoside; 6, iriflophenone 3-C-(2-O-galloyl)---D-glucoside; 7, methyl-iriflophenone 3-C-(2,6-di-O-galloyl)---D-glucoside) and xanthones (4, mangiferin and 8, 6-O-galloyl-mangiferin). The estrogenic and antioxidant effects of aqueous extracts from Mangifera indica L. cv. "Kent" leaves on ovariectomized rats were determined by uterotrophic assay and malondialdehyde (MDA) levels in erythrocytes, bone, liver, and stomach. We conclude that the polyphenolic compounds from extracts act as exogenous antioxidant agents against oxidative damage in ovariectomized rats.


La composición química de las hojas de Mangifera indica L. cv. "Kent" se determinó por HPLC-ESI-QTOF-MS/MS. Compuestos polifenólicos caracterizados como derivados de benzofenona fueron los componentes principales encontrados en los extractos (1, isómero de la maclurina 3-C-(2-O-galoyil)-D-glucósido; 2, maclurina 3-C-ß-D-glucósido; 3, iriflofenona 3-C-ß-D-glucósido; 5, maclurina 3-C-(2,3-di-O-galloíl)-ß-D-glucósido; 6, iriflofenona 3-C-(2-O-galloil)-ß-D-glucósido; 7, metil-iriflofenona 3-C-(2,6-di-O- galloyl)-ß-D-glucósido) y xantonas (4, mangiferina y 8, 6-O-galoyil-mangiferina). Los efectos estrogénicos y antioxidantes de los extractos acuosos de hojas de Mangifera indica L. cv. "Kent" en ratas ovariectomizadas se determinaron mediante ensayo uterotrófico y la medición de los niveles de malondialdehído (MDA) en eritrocitos, huesos, hígado y estómago. Concluimos que los compuestos polifenólicos de los extractos actúan como agentes antioxidantes exógenos contra el daño oxidativo en ratas ovariectomizadas.


Subject(s)
Animals , Female , Rats , Plant Extracts/pharmacology , Plant Extracts/chemistry , Ovariectomy , Mangifera/chemistry , Estrogens/pharmacology , Antioxidants/pharmacology , Stomach/drug effects , Benzophenones/chemistry , Bone and Bones/drug effects , Lipid Peroxidation/drug effects , Chromatography, High Pressure Liquid , Reactive Oxygen Species , Rats, Sprague-Dawley , Plant Leaves/chemistry , Spectrometry, Mass, Electrospray Ionization , Ethanol , Tandem Mass Spectrometry , Liver/drug effects , Malondialdehyde , Antioxidants/chemistry
11.
Arq. neuropsiquiatr ; 77(2): 106-114, Feb. 2019. tab, graf
Article in English | LILACS | ID: biblio-983892

ABSTRACT

ABSTRACT Ducrosia anethifolia has been recommended as a remedy for neurological disorders. However, the anticonvulsant effects of D. anethifolia essential oil (DAEO) and its major constituent α-pinene have not yet been clarified. Methods: A rat model of pentylenetetrazole (PTZ)-induced convulsions was used. Oxidant and antioxidant parameters were assayed in the temporal lobe. Results: The data showed that DAEO (50, 100 and 200 mg/kg, i.p.) and α-pinene (0.2 and 0.4 mg/kg i.p.) delayed the initiation time, and reduced the duration of myoclonic and tonic-clonic seizures following PTZ injection. The PTZ produced oxidative stress so that malondialdehyde and hydrogen peroxide levels were increased and catalase and peroxidase activity decreased. Pretreatment with DAEO and α-pinene significantly inhibited the above-mentioned enzymatic changes in PTZ-treated animals. Conclusion: The results suggest that α-pinene, at teast in part, was responsible for the induction of the anticonvulsant and antioxidant effects of DAEO in rats.


RESUMO A Ducrosia anethifolia tem sido recomendada como remédio para os distúrbios neurológicos. No entanto, os efeitos anticonvulsivantes do óleo essencial de Ducrosia anethifolia (DAEO) e do seu principal constituinte atfa-pineno (α-pineno) ainda não foram clarificados. Métodos: Foi utilizado um modelo de rato de convulsões induzidas por pentilenotetrazol (PTZ). Os parâmetros oxidante e antioxidante foram ensaiados no lobo temporal do cérebro. Resultados: Os dados mostraram que DAEO (50, 100 e 200 mg / kg, i.p.) e α-pineno (0,2 e 0,4 mg / kg i.p.) retardaram o tempo de iniciação e reduziram a duração das crises mioclônicas e tônico-clônicas após a injeção de PTZ. O PTZ produziu estresse oxidativo, de modo que os níveis de malondialdeído (MDA) e de peróxido de hidrogênio aumentaram e a atividade da catalase e da peroxidase diminuiu. O pré-tratamento com DAEO e α-pineno inibiu significativamente as alterações enzimáticas mencionadas em animais tratados com PTZ. Conclusão: O resultado sugere que α-pineno, peto menos em parte, é responsável peta indução dos efeitos anticonvulsivantes e antioxidantes da DAEO em ratos.


Subject(s)
Animals , Male , Seizures/drug therapy , Oils, Volatile/pharmacology , Apiaceae/chemistry , Bicyclic Monoterpenes/pharmacology , Anticonvulsants/pharmacology , Pentylenetetrazole , Seizures/metabolism , Time Factors , Oils, Volatile/chemistry , Lipid Peroxidation/drug effects , Catalase/analysis , Reproducibility of Results , Chromatography, High Pressure Liquid , Treatment Outcome , Rats, Wistar , Peroxidase/analysis , Oxidative Stress/drug effects , Bicyclic Monoterpenes/chemistry , Hydrogen Peroxide/analysis , Malondialdehyde/analysis , Anticonvulsants/chemistry , Antioxidants/analysis , Antioxidants/metabolism
12.
Article in English | WPRIM | ID: wpr-719637

ABSTRACT

Oxidative stress is considered a major contributor in the pathogenesis of diabetic neuropathy and in diabetes complications, such as nephropathy and cardiovascular diseases. Diabetic neuropathy, which is the most frequent complications of diabetes, affect sensory, motor, and autonomic nerves. This study aimed to investigate whether 7,8-dihydroxyflavone (7,8-DHF) protects SH-SY5Y neuronal cells against high glucose-induced toxicity. In the current study, we found that diabetic patients exhibited higher lipid peroxidation caused by oxidative stress than healthy subjects. 7,8-DHF exhibits superoxide anion and hydroxyl radical scavenging activities. High glucose-induced toxicity severely damaged SH-SY5Y neuronal cells, causing mitochondrial depolarization; however, 7,8-DHF recovered mitochondrial polarization. Furthermore, 7,8-DHF effectively modulated the expression of pro-apoptotic protein (Bax) and anti-apoptotic protein (Bcl-2) under high glucose, thus inhibiting the activation of caspase signaling pathways. These results indicate that 7,8-DHF has antioxidant effects and protects cells from apoptotic cell death induced by high glucose. Thus, 7,8-DHF may be developed into a promising candidate for the treatment of diabetic neuropathy.


Subject(s)
Antioxidants , Autonomic Pathways , Cardiovascular Diseases , Cell Death , Diabetes Complications , Diabetic Neuropathies , Glucose , Healthy Volunteers , Humans , Hydroxyl Radical , Lipid Peroxidation , Neurons , Oxidative Stress , Superoxides
13.
Article in English | WPRIM | ID: wpr-764958

ABSTRACT

BACKGROUND: Removal of uremic toxins such as indoxyl sulfate by AST-120 is known to improve renal function and delay the initiation of dialysis in patients with advanced chronic kidney disease. However, it is unclear whether the addition of AST-120 to conventional treatments is effective in delaying the progression of renal dysfunction in patients with diabetic nephropathy. METHODS: A total of 100 patients with type 2 diabetes and renal dysfunction (serum creatinine levels ranging from 1.5 to 3.0 mg/dL) were recruited from eight centers in Korea and treated with AST-120 (6 g/day) for 24 weeks. The primary endpoint was improvement in renal function measured as the gradient of the reciprocal serum creatinine level (1/sCr) over time (i.e., the ratio of 1/sCr time slope for post- to pre-AST-120 therapy). A response was defined as a ratio change of the regression coefficient of 1/sCr ≤ 0.90. RESULTS: Renal function improved in 80.3% of patients (61/76) after 24 weeks of AST-120 treatment. There were no differences between responder and non-responder groups in baseline characteristics except for diastolic blood pressure (73.5 ± 9.5 mmHg in the responder group vs. 79.3 ± 11.1 mmHg in the non-responder group; P = 0.046). Serum lipid peroxidation level decreased significantly in the responder group (from 2.25 ± 0.56 μmol/L to 1.91 ± 0.72 μmol/L; P = 0.002) but not in the non-responder group. CONCLUSION: The addition of AST-120 to conventional treatments may delay the progression of renal dysfunction in diabetic nephropathy. The antioxidant effect of AST-120 might contribute to improvement in renal function.


Subject(s)
Antioxidants , Blood Pressure , Creatinine , Diabetic Nephropathies , Dialysis , Humans , Indican , Korea , Lipid Peroxidation , Oxidative Stress , Prospective Studies , Renal Insufficiency, Chronic
14.
Article in Chinese | WPRIM | ID: wpr-773691

ABSTRACT

The aim of this paper was to compare the performance of acute liver injury in mice induced by Tripterygium Glycosides Tablets from 6 different manufacturers,and to explore the toxicity mechanism from the perspective of oxidative stress and apoptosis preliminarily. Male or female mice were randomly divided into normal group,Zhejiang group,Hunan group,Hubei group,Shanghai group,Jiangsu group and Fujian group. Mice in Tripgerygium Glycosides Tablets groups were given 16 times the clinical equivalent dose( 300 mg·kg-1) Tripgerygium Glycosides Tablets by oral administration for one time,mice were executed in 24 h after lavaged.Then the visceral brain coefficient of the organ was calculated. Histopathological changes of liver were observed by hematoxylin-eosin staining. Td T-mediated d UTP nick-end labeling was used to detect the apoptosis of the liver cells and the protein content of oxidative stress related factors in liver homogenate. Nuclear transcription factor E2-related factor( Nrf2) and heme oxygenase-1( HO-1) as well as mitochondrial mediated apoptosis-related protein expression levels of Bax and Bcl-2 in hepatic tissue were measured by Western blot.Within 24 hours of administration,6 male mice in Jiangsu group and 2 female mice in Zhejiang group were dying; compared with normal ones,liver coefficients of mice in Zhejiang,Shanghai,Jiangsu and Hunan groups were significantly increased,thymus coefficients in the first two groups were significantly reduced,as well as the lung coefficients of Fujian group mice,the rest was normal. In addition to Hubei group,serum AST,ALT or ALP levels of mice were increased,while TBi L were not being affected. Histopathological changes and apoptosis of liver cells were observed in all mice,and the degree of severity was ranked as Jiangsu,Zhejiang,Shanghai,Hunan,Hubei and Fujian group. All Tripterygium Glycosides Tablets increased the MDA and reduced the content of T-SOD,CAT or GSH in liver tissue while inhibited Nrf2,HO-1 and Bcl-2,increased the protein expression level of Bax( except Hunan group). Tripgerygium Glycosides Tablets from 6 manufacturers all resulted in liver function damage and liver histopathological changes,especially in Jiangsu,Hubei and Fujian,and the mechanism may related to inhibit Nrf2/HO-1 oxidative stress pathway and activate Bax/Bcl-2 apoptosis pathway to mediate lipid peroxidation and induce liver cell apoptosis. Triptolide A may be one of the main toxic components of Tripgerygium Glycosides Tablets that causing drug-induced liver injury. This study was conducted on normal mice with super dose medication,so the relevant results are for reference only.


Subject(s)
Animals , Apoptosis , Chemical and Drug Induced Liver Injury , Drugs, Chinese Herbal , Toxicity , Female , Glycosides , Toxicity , Heme Oxygenase-1 , Metabolism , Lipid Peroxidation , Liver , Male , Membrane Proteins , Metabolism , Mice , NF-E2-Related Factor 2 , Metabolism , Oxidative Stress , Proto-Oncogene Proteins c-bcl-2 , Metabolism , Random Allocation , Tablets , Tripterygium , Toxicity , bcl-2-Associated X Protein , Metabolism
15.
Article in Chinese | WPRIM | ID: wpr-773652

ABSTRACT

The aim of this paper was to investigate the molecular mechanism of Calculus Bovis Sativus( CBS) in alleviating lipid accumulation in vitro by serum pharmacology. The CBS-containing serum of mice was obtained by serum pharmacology method to evaluate its effect on the proliferation of LO2 hepatocytes. The lipid reducing effects of CBS-containing serum through Nrf2 was evaluated by fructose-induced LO2 hepatocyte steatosis model,nuclear factor erythroid 2 related factor 2( Nrf2) agonist oltipraz combined intervention,cell oil red O staining and intracellular triglyceride( TG) content. The effects of CBS-containing serum on lipid peroxidation and hepatocytes apoptosis were evaluated by reactive oxygen species( ROS) and apoptosis assay,respectively. Real-time quantitative polymerase chain reaction( PCR) was used to detect the relative expression of lipid synthesis-related genes and apoptosis-related genes.RESULTS:: showed that CBS drug-containing serum had no significant effect on LO2 hepatocyte proliferation. As compared with the model group,CBS-containing serum could effectively reduce the formation of lipid droplets in fructose-induced LO2 hepatocytes,significantly reduce intracellular TG and ROS levels,and significantly reduce hepatocyte apoptosis rate( P < 0. 05). As compared with the model group,carbohydrate responsive element binding protein( ChREBP),sterol regulatory element binding protein-1 c( SREBP-1 c),fatty acid synthase( FAS),acetyl-CoA carboxylase 1( ACC1),stearoyl-CoA desaturase 1( SCD1),Bax and caspase-3 mRNA levels were significantly reduced in CBS drug-containing serum treatment group( P<0. 05). All of the above effects could be reversed by oltipraz.In conclusion,CBS-containing serum can significantly inhibit the fructose-induced LO2 liver fat deposition,and the mechanism may be related to reducing intracellular ROS level through the Nrf2 pathway and improving intracellular peroxidation state to reduce apoptosis.


Subject(s)
Animals , Apoptosis , Cattle , Cells, Cultured , Fatty Liver , Fructose , Gallstones , Chemistry , Hepatocytes , Cell Biology , Metabolism , Lipid Metabolism , Lipid Peroxidation , Liver , Medicine, Chinese Traditional , Mice , Reactive Oxygen Species , Metabolism , Serum , Chemistry , Sterol Regulatory Element Binding Protein 1 , Metabolism , Triglycerides
16.
Article in English | WPRIM | ID: wpr-758886

ABSTRACT

In vitro prediction of hepatotoxicity can enhance the performance of non-clinical animal testing for identifying chemical hazards. In this study, we assessed high-content analysis (HCA) using multi-parameter cell-based assays as an in vitro hepatotoxicity testing model using various hepatotoxicants and human hepatocytes such as HepG2 cells and human primary hepatocytes (hPHs). Both hepatocyte types were exposed separately to multiple doses of ten hepatotoxicants associated with liver injury whose mechanisms of action have been described. HCA data were obtained using fluorescence probes for nuclear size (Hoechst), mitochondrial membrane potential (TMRM), cytosolic free calcium (Fluo-4AM), and lipid peroxidation (BODIPY). Cellular alterations were observed in response to all hepatotoxicants tested. The most sensitive parameter was TMRM, with high sensitivity at a low dose, next was BODIPY, followed by Fluo-4AM. HCA data from HepG2 cells and hPHs were generally concordant, although some inconsistencies were noted. Both hepatocyte types showed mild or severe mitochondrial impairment and lipid peroxidation in response to several hepatotoxicants. The results demonstrate that the application of HCA to in vitro hepatotoxicity testing enables more efficient hazard identification, and further, they suggest that certain parameters could serve as sensitive endpoints for predicting the hepatotoxic potential of chemical compounds.


Subject(s)
Animals , Calcium , Cytosol , Fluorescence , Hep G2 Cells , Hepatocytes , Humans , In Vitro Techniques , Lipid Peroxidation , Liver , Membrane Potential, Mitochondrial
17.
Laboratory Animal Research ; : 107-113, 2019.
Article in English | WPRIM | ID: wpr-786397

ABSTRACT

Acetaminophen (APAP) is the most common antipyretic analgesic worldwide. However, APAP overdose causes severe liver injury, especially centrilobular necrosis, in humans and experimental animals. At therapeutic dosage, APAP is mainly metabolized by sulfation and glucuronidation, and partly by cytochrome P450–mediated oxidation. However, APAP overdose results in production of excess reactive metabolite, N-acetyl-p-benzoquinone imine (NAPQI), by cytochromes P450; NAPQI overwhelms the level of glutathione (GSH), which could otherwise detoxify it. NAPQI binds covalently to proteins, leading to cell death. A number of studies aimed at the prevention and treatment of APAP-induced toxicity are underway. Rats are more resistant than mice to APAP hepatotoxicity, and thus mouse models are mainly used. In the present study, we compared the toxic responses induced by APAP overdose in the liver of ICR mice obtained from three different sources and evaluated the usability of the Korl:ICR stock established by the National Institute of Food and Drug Safety Evaluation in Korea. Administration of APAP (300 mg/kg) by intraperitoneal injection into male ICR mice enhanced CYP2E1 protein expression and depleted hepatic GSH level 2 h after treatment accompanied with significantly increased level of hepatic malondialdehyde, a product of lipid peroxidation. Regardless of the source of the mice, hepatotoxicity, as evidenced by activity of serum alanine aminotransferase, increased from 8 h and peaked at 24 h after APAP treatment. In summary, hepatotoxicity was induced after the onset of oxidative stress by overdose of APAP, and the response was the same over time among mice of different origins.


Subject(s)
Acetaminophen , Alanine Transaminase , Animals , Cell Death , Cytochrome P-450 CYP2E1 , Cytochromes , Glutathione , Humans , Injections, Intraperitoneal , Korea , Lipid Peroxidation , Liver , Male , Malondialdehyde , Mice , Mice, Inbred ICR , Necrosis , Oxidative Stress , Rats
18.
Clinics ; 74: e787, 2019. graf
Article in English | LILACS | ID: biblio-1011911

ABSTRACT

OBJECTIVES: Intestinal obstruction has a high mortality rate when therapeutic treatment is delayed. Resuscitation in intestinal obstruction requires a large volume of fluid, and fluid combinations have been studied. Therefore, we evaluated the effects of hypertonic saline solution (HS) with pentoxifylline (PTX) on apoptosis, oxidative stress and survival rate. METHODS: Wistar rats were subjected to intestinal obstruction and ischemia through a closed loop ligation of the terminal ileum and its vessels. After 24 hours, the necrotic bowel segment was resected, and the animals were randomized into four groups according to the following resuscitation strategies: Ringer's lactate solution (RL) (RL-32 ml/kg); RL+PTX (25 mg/kg); HS+PTX (HS, 7.5%, 4 ml/kg), and no resuscitation (IO-intestinal obstruction and ischemia). Euthanasia was performed 3 hours after resuscitation to obtain kidney and intestine samples. A malondialdehyde (MDA) assay was performed to evaluate oxidative stress, and histochemical analyses (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling [TUNEL], Bcl-2 and Bax) were conducted to evaluate kidney apoptosis. Survival was analyzed with another series of animals that were observed for 15 days. RESULTS: PTX in combination with RL or HS reduced the MDA levels (nmol/mg of protein), as follows: kidney IO=0.42; RL=0.49; RL+PTX=0.31; HS+PTX=0.34 (p<0.05); intestine: IO=0.42; RL=0.48; RL+PTX=0.29; HS+PTX=0.26 (p<0.05). The number of labeled cells for TUNEL and Bax was lower in the HS+PTX group than in the other groups (p<0.05). The Bax/Bcl-2 ratio was lower in the HS+PTX group than in the other groups (p<0.05). The survival rate on the 15th day was higher in the HS+PTX group (77%) than in the RL+PTX group (11%). CONCLUSION: PTX in combination with HS enhanced survival and attenuated oxidative stress and apoptosis. However, when combined with RL, PTX did not reduce apoptosis or mortality.


Subject(s)
Animals , Male , Pentoxifylline/pharmacology , Resuscitation/methods , Saline Solution, Hypertonic/pharmacology , Apoptosis/drug effects , Oxidative Stress/drug effects , Intestinal Obstruction/metabolism , Immunohistochemistry , Lipid Peroxidation/drug effects , Random Allocation , Reproducibility of Results , Rats, Wistar , In Situ Nick-End Labeling , Disease Models, Animal , Kaplan-Meier Estimate , Intestinal Obstruction/mortality , Intestinal Obstruction/prevention & control , Intestine, Small/drug effects , Intestine, Small/metabolism , Kidney/drug effects , Kidney/metabolism , Malondialdehyde/analysis
19.
Clinics ; 74: e658, 2019. tab, graf
Article in English | LILACS | ID: biblio-989637

ABSTRACT

OBJECTIVES Vascular endothelial growth factor (VEGF) and its receptors play important roles in angiogenesis. Melatonin plays an important role in gonadal development; thus, its effect on the reproductive system is evident. We investigated the influence of melatonin on the expression of VEGF, vascular endothelial growth factor receptor-1 (VEGFR1) and vascular endothelial growth factor receptor-2 (VEGFR2), as well as on changes in oxidative stress markers and follicle numbers in rat ovaries. METHODS For this purpose, 45 Wistar rats were separated into the following groups: Group 1, control; Group 2, vehicle; and Group 3, melatonin. Rats in Group 3 were treated with melatonin at 50 mg/kg/day for 30 days. The effects of melatonin on the expression of VEGF, VEGFR1 and VEGFR2 were established by immunohistochemistry analysis. The effects of melatonin on antioxidant enzyme activities were demonstrated by spectrophotometric analysis. RESULTS Based on immunohistochemistry analysis, VEGFR2 was predominantly localized to theca cells in the ovary. Our data indicate that melatonin treatment can significantly increase VEGF and VEGFR1 expression in the ovary ( p <0.05). Additionally, the number of degenerated follicles significantly decreased with melatonin treatment ( p <0.05). Melatonin administration also led to significant increases in antioxidant enzyme levels in the ovary. CONCLUSION Melatonin treatment exerts protective effects on follicles against increased lipid peroxidation through modulating tissue antioxidant enzyme levels. These effects may be related to angiogenesis and antioxidant activities.


Subject(s)
Animals , Female , Ovary/drug effects , Neovascularization, Physiologic/drug effects , Vascular Endothelial Growth Factor Receptor-2/drug effects , Vascular Endothelial Growth Factor A/drug effects , Melatonin/pharmacology , Antioxidants/pharmacology , Ovary/enzymology , Ovary/blood supply , Superoxide Dismutase/metabolism , Lipid Peroxidation , Catalase/metabolism , Rats, Wistar , Models, Animal , Malondialdehyde/metabolism , Melatonin/metabolism , Antioxidants/metabolism
20.
Int. j. morphol ; 37(1): 65-70, 2019. graf
Article in English | LILACS | ID: biblio-990006

ABSTRACT

SUMMARY: Valproic acid (VPA), an antiepileptic drug, has been demonstrated to damage histology and to change tyrosine phosphorylation patterns with increased oxidative stress in perirenal tissues. This study aimed to investigate the effect of VPA on microstructure, tyrosine phosphorylation, and lipid peroxidation of rat kidney. Adult male rats were divided into control and VPA-treated groups intraperitoneally injected with normal saline and VPA 500 mg/kgBW for 10 consecutive days, respectively (n = 7 each). The blood serum was examined for biochemical levels. The kidney tissues were routinely processed for histological observation. Total proteins from kidney were extracted to assay the malondialdehyde (MDA) levels and phosphorylation expression. The results showed that VPA significantly decreased blood glucose levels while tend to increase urea nitrogen and creatinine. MDA levels in VPA group were significantly higher that of control. Renal cortex of VPA-treated animals revealed vasodilatations. Although the ratio of a renal phosphorylated 72 kDa protein/ beta actin expression seemed to be not different in both groups, VPA significantly decreased the intensity of beta actin. In conclusion, VPA dilates renal microvasculature with increasing of MDA but suppresses the actin expression.


RESUMEN: Se ha demostrado que el ácido valproico (AVP), un fármaco antiepiléptico, daña la histología y cambia los patrones de fosforilación de la tirosina con el aumento del estrés oxidativo en los tejidos perirrenales. Este estudio tuvo como objetivo investigar el efecto del AVP en la microestructura, la fosforilación de la tirosina y la peroxidación lipídica del riñón de rata. Se dividieron ratas macho adultas en grupos control y tratados con AVP. Durante 10 días consecutivos fueron inyectadas por vía intraperitoneal con solución salina normal y 500 mg / kg de PC respectivamente (n = 7 cada uno). Se analizó el suero sanguíneo para determinar los niveles bioquímicos. Los tejidos renales se procesaron de forma rutinaria para la observación histológica. Las proteínas totales del riñón se extrajeron para analizar los niveles de malondialdehído (MDA) y la expresión de la fosforilación. Los resultados mostraron que el AVP disminuyó significativamente los niveles de glucosa en la sangre, mientras que tienden a aumentar el nitrógeno ureico y la creatinina. Los niveles de MDA en el grupo de AVP fueron significativamente más altos que los del control. La corteza renal de los animales tratados con AVP reveló vasodilataciones. Aunque la proporción de una expresión de proteína / actina de 72 kDa fosforilada renal no parece ser diferente en ambos grupos, el AVP disminuyó significativamente la intensidad de la actina beta. En conclusión, el AVP dilata la microvasculatura renal al aumentar el MDA, pero suprime la expresión de actina.


Subject(s)
Animals , Male , Rats , Tyrosine/drug effects , Lipid Peroxidation/drug effects , Valproic Acid/pharmacology , Kidney/drug effects , Anticonvulsants/pharmacology , Organ Size , Phosphorylation , Vasodilation/drug effects , Blotting, Western , Rats, Wistar , Electrophoresis, Polyacrylamide Gel , Malondialdehyde
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