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1.
Article in English | WPRIM | ID: wpr-881039

ABSTRACT

A contributory role of oxidative stress and protection by antioxidant nutrients have been suspected in cataract formation. Ganoderic acid A (GAA), an effective lanostane triterpene, is widely reported as an antioxidant. The aim of this study is to investigate the potential effects of GAA on cataract formation. After lens epithelial cells (LECs) were exposed to UVB radiation for different periods, cell viability, apoptosis-related protein levels, malondialdehyde (MDA) and superoxide dismutase (SOD) activities were monitored. We found that cell viability, the Bcl-2/Bax ratio and SOD activity were increased, while Cleaved caspase-3 levels and MDA activity were decreased compared with those in UVB-impaired LECs after GAA treated. Furthermore, GAA activated PI3K/AKT in UVB-impaired LECs and effectively delayed the occurrence of lens opacity in vitro. In conclusion, these findings demonstrated that GAA exhibited protective functions in SRA01/04 cells and rat lenses against UVB-evoked impairment through elevating cell viability and antioxidant activity, inhibiting cell apoptosis, activating the PI3K/AKT pathway and delaying lens opacity.


Subject(s)
Animals , Apoptosis , Cataract/prevention & control , Cell Line , Cell Survival , Epithelial Cells/radiation effects , Heptanoic Acids/pharmacology , Humans , Lanosterol/pharmacology , Lens, Crystalline/radiation effects , Malondialdehyde/metabolism , Rats , Superoxide Dismutase/metabolism , Ultraviolet Rays/adverse effects
2.
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
3.
Rev. chil. cardiol ; 37(2): 93-103, ago. 2018. tab, graf, ilus
Article in Spanish | LILACS | ID: biblio-959346

ABSTRACT

Resumen: Introducción: El ejercicio físico reduce la mortalidad cardiovascular y genera remodelado cardíaco. Altas cargas de entrenamiento pueden generar remodelado cardíaco adverso. Biomarcadores (BMC) de inflamación Interleukina 6 (IL-6) y de estrés oxidativo Malondialdehído (MDA), potencialmente pueden caracterizar la respuesta al esfuerzo. Objetivo: Evaluar actividad de IL-6 y MDA en respuesta a una maratón en atletas con distinto nivel de entrenamiento y remodelado cardíaco asociado. Sujetos y Métodos: Estudio prospectivo, simple ciego, incluyó 16 atletas que completaron la maratón de Santiago (42 k), separados según entrenamiento previo, grupo 1 (G1, n: 8): Alto ≥ 100 km/semana y grupo 2 (G2, n: 8): Bajo <100 km/semana). Se obtuvo pre y post maratón: niveles de IL-6, MDA y ecocardiografía Doppler transtorácica (ETT); cuantificando cámaras cardíacas izquierdas, derechas y deformación del ventrículo izquierdo (strain longitudinal). Se utilizaron las pruebas de Mann-Whitney, Wilcoxon y Kruskal-Wallis. Resultados: Edad G1: 38.13±7.18 años vs G2: 40.38±6.63 años (NS). Tiempo maratón G1: 185.75±14.87 min vs G2: 219.75±24.92 min (p<0.01). Masa del ventrículo izquierdo G1: 91±21 g/m2 vs G2: 73±12 g/m2 (p<0.01). Volumen aurícula izquierda G1: 39.4±12.6 ml/m2 vs 30.6±4.6 ml/m2 (p<0.01). FEVI G1: 55.8±3.3% vs G2: 58.6±6.7% (NS). MDA G1: PRE 0.17±0.13 uM/L, POST 0.67±0.59 uM/L, G2: PRE 0.29±0.24 uM/L, POST 1.01±1.15 uM/L (p<0.01). IL-6 G1: PRE 2.50±1.35 pg/ml, POST 93.91±27.23 pg/ml vs G2: PRE 4.65±5.89 pg/ml, POST 97.83±30.72 pg/ml (NS). Conclusión: El ejercicio físico aumenta los BMC de inflamación y estés oxidativo (IL-6, MDA). Un entrenamiento físico de alta intensidad disminuye la respuesta de estrés oxidativo y se asocia a un mayor remodelado cardíaco.


Abstract: Background: Exercise reduces cardiovascular mortality and generates cardiac remodeling. High training loads can induce adverse cardiac remodeling, and its associated cardiac remodeling. Therefore, interleukin 6 (IL 6) and malondialdehyde (MDA), biomarkers of inflammatory response and oxidative stress respectively, may have a role in stratifying this risk. Objective: To assess the activity of IL-6 and MDA in response to a marathon race in athletes with different previous training status. Subjects And Methods: Prospective, single-blind study involving 16 male athletes that finished the Santiago Marathon (42 k), allocated into two groups according to their previous training: Group 1 (G1, n: 8) with high training (≥ 100 km/weekly) and Group 2 (G2, n: 8) with low training (< 100 km/weekly). Before and after the race serum levels of IL-6, MDA and transthoracic Doppler echocardiography for cardiac chamber quantification and left ventricle deformation (longitudinal strain) were measured. Mann-Whitney, Wilcoxon, and Kruskal-Wallis tests were used to assess statistical significance. Results: Age G1: 38.13±7.18 years-old vs G2: 40.38±6.63 years-old (NS). Marathon finishing time G1: 185.75±14.87 min vs G2: 219.75±24.92 min (p<0.01). Left ventricle mass G1: 91±21 g/m2 vs G2: 73±12 g/m2 (p<0.01). Left atrium volume G1: 39.4±12.6 ml/m2 vs 30.6±4.6 ml/m2 (p<0.01). LVEF G1: 55.8±3.3% vs G2: 58.6±6.7% (NS). MDA G1: PRE 0.17±0.13 uM/L, POST 0.67±0.59 uM/L, G2: PRE 0.29±0.24 uM/L, POST 1.01±1.15 uM/L (p<0.01). IL-6 G1: PRE 2.50±1.35 pg/ml, POST 93.91±27.23 vs G2: PRE 4.65±5.89 pg/ml, POST 97.83±30.72 pg/ml (NS). Conclusion: Physical exercise generates a rise in biomarkers (IL-6, MDA). Athletes with high-intensity training level have a diminished oxidative stress response post effort and greater cardiac remodeling.


Subject(s)
Humans , Male , Adolescent , Adult , Middle Aged , Young Adult , Interleukin-6/metabolism , Ventricular Remodeling/physiology , Exercise Therapy/methods , Malondialdehyde/metabolism , Echocardiography , Biomarkers , Single-Blind Method , Prospective Studies , Oxidative Stress/physiology , Athletes , Heart Ventricles/diagnostic imaging
4.
Acta cir. bras ; 33(7): 556-564, July 2018. tab, graf
Article in English | LILACS | ID: biblio-949368

ABSTRACT

Abstract Purpose: To investigate the effects of baicalin on inflammatory reaction, oxidative stress and protein kinase D1 (PKD1) and nuclear factor-kappa B (NF-κB) protein expressions in severe acute pancreatitis (SAP) rats. Methods: Sixty rats were divided into sham operation, model, and low-, medium- and high-dose baicalin group. SAP model was established in later 4 groups. The later 3 groups were injected with 0.1, 0.2 and 0.4 ml/100 g 5% baicalin injection, respectively. At 12 h, the serum SAP related indexes and inflammatory factors, peripheral blood CD3 and γδT cell percentages, wet/dry ratio and pancreas ascites volume, oxidative stress indexes and PKD1 and NF-κB protein expressions in pancreatic tissue were determined. Results: Compared with model group, in high-dose baicalin group the wet/dry ratio and ascites volume, serum amylase level, phospholipase A2 activity, TNF-α, IL-1 and IL-6 levels, and pancreatic malondialdehyde level and PKD1 and NF-κB protein expression were significantly decreased (P < 0.05), and peripheral blood CD3 and γδT cell percentages and pancreatic superoxide dismutase and glutathione peroxidase levels were significantly increased (P < 0.05). Conclusion: Baicalin can resist the inflammatory reaction and oxidative stress, and down-regulate protein kinase D1 and nuclear factor-kappa B protein expressions, thus exerting the protective effects on severe acute pancreatitis in rats.


Subject(s)
Animals , Pancreatitis/drug therapy , Flavonoids/pharmacology , Protein Kinase C/metabolism , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , NF-kappa B/metabolism , Oxidative Stress/drug effects , Pancreatitis/metabolism , Superoxide Dismutase/drug effects , Protein Kinase C/drug effects , Random Allocation , Down-Regulation/drug effects , Reproducibility of Results , NF-kappa B/drug effects , Interleukin-6/blood , Interleukin-1/blood , Tumor Necrosis Factor-alpha/blood , Treatment Outcome , Rats, Sprague-Dawley , CD3 Complex/drug effects , CD3 Complex/blood , Glutathione Peroxidase/drug effects , Glutathione Peroxidase/metabolism , Amylases/drug effects , Amylases/blood , Malondialdehyde/metabolism
5.
Acta cir. bras ; 33(3): 197-206, Mar. 2018. graf
Article in English | LILACS | ID: biblio-886272

ABSTRACT

Abstract Purpose: To evaluate whether their combination was more effective than either alone in decreasing renal damage due to ischemia/reperfusion (I/R) injury in rats. Methods: Thirty-two Wistar rats were assigned to four groups. Following right nephrectomy, their left kidneys were subjected to warm ischemia (IR), cold ischemia (TH+IR), intraperitoneal injection of 10 mg/kg melatonin (MEL+IR), or injection of 10 mg/kg melatonin followed by cold ischemia (MEL+TH+IR). Eight randomly assigned right kidneys constituted the control group. After 240 min of reperfusion, left nephrectomy was performed for histopathological evaluation, lipid peroxidation, and measurement of antioxidant enzyme activity. Serum was collected to measure urea and creatinine concentrations. Results: Histopathological damage induced by ischemia and reperfusion was more attenuated in the MEL+TH+IR group than in the MEL+IR and TH+IR groups (p<0.037). Superoxide dismutase activity was significantly higher (p<0.029) and creatinine (p<0.001) and urea (p<0.001) concentrations were significantly lower in the MEL+TH+IR group than in the MEL+IR and TH+IR groups. Conclusion: The combination of melatonin (MEL) and topical hypothermia (TH) better protects against renal I/R injury than does MEL or TH alone.


Subject(s)
Animals , Male , Rats , Reperfusion Injury/prevention & control , Hypothermia, Induced/methods , Kidney/blood supply , Melatonin/therapeutic use , Superoxide Dismutase/metabolism , Reperfusion Injury/pathology , Rats, Wistar , Combined Modality Therapy , Oxidative Stress , Disease Models, Animal , Malondialdehyde/metabolism
6.
Braz. j. med. biol. res ; 51(10): e7439, 2018. graf
Article in English | LILACS | ID: biblio-951707

ABSTRACT

Nuclear factor erythroid-related factor 2 (Nrf2) has been implicated in several detoxifying and antioxidant defense processes. Nrf2-mediated heme oxygenase-1 (HO-1) expression was demonstrated to play a key role against oxidative stress. Gastrodin (GSTD) is a well-known active compound isolated from the roots of Rhizoma gastrodiae, a plant used in ancient Chinese traditional medicine. The aim of this work was to investigate whether GSTD could alleviate H2O2-induced oxidative stress in mouse liver sinusoidal endothelial cells (LSECs). In LSECs exposed to 1 mM H2O2, treatment with GSTD (1, 10, or 50 µM) resulted in higher cell viability than the untreated control. Treated cells maintained a higher Bcl2/Bax ratio and suppressed caspase-9 expression compared with untreated cells, reducing cell apoptosis. GSTD was protective for H2O2-induced oxidative injury by reducing the generation of intracellular reactive oxygen species and malondialdehyde. HO-1 and Nrf2 expressions were synergistically upregulated by GSTD. Inhibition of HO-1 by 10 µM zinc protoporphyrin resulted in less protective effects on cell viability and malondialdehyde reduction by GSTD treatment in H2O2-exposed LSECs. Additionally, phosphorylated p38 in LSECs exposed to H2O2 was elevated by GSTD. Inhibition of p38 phosphorylation by SB203580 did not induce Nrf2 and HO-1 expression after 1 or 10 µM GSTD treatment and the protective effect on cell viability and malondialdehyde reduction in H2O2-exposed LSECs was reduced. The data conclusively demonstrated that GSTD-induced HO-1 and Nrf2 expression is involved in protection of LSECs from H2O2-induced oxidative injury, which may be regulated by p38 phosphorylation.


Subject(s)
Animals , Rabbits , Benzyl Alcohols/pharmacology , Endothelial Cells/drug effects , p38 Mitogen-Activated Protein Kinases/metabolism , Heme Oxygenase-1/metabolism , Glucosides/pharmacology , Hydrogen Peroxide/pharmacology , Up-Regulation/drug effects , Cell Survival/drug effects , Apoptosis/drug effects , Liver/cytology , Liver/drug effects , Malondialdehyde/metabolism , Models, Theoretical
7.
Braz. j. med. biol. res ; 51(6): e6555, 2018. graf
Article in English | LILACS | ID: biblio-889109

ABSTRACT

Long non-coding RNAs (lncRNAs) play an important role in the pathogenesis of cardiovascular diseases, especially in myocardial infarction and ischemia/reperfusion (I/R). However, the underlying molecular mechanism remains unclear. In this study, we determined the role and the possible underlying molecular mechanism of lncRNA-ROR in myocardial I/R injury. H9c2 cells and human cardiomyocytes (HCM) were subjected to either hypoxia/reoxygenation (H/R), I/R or normal conditions (normoxia). The expression levels of lncRNA-ROR were detected in serum of myocardial I/R injury patients, H9c2 cells, and HCM by qRT-PCR. Then, levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) were measured by kits. Cell viability, apoptosis, apoptosis-associated factors, and p38/MAPK pathway were examined by MTT, flow cytometry, and western blot assays. Furthermore, reactive oxygen species (ROS) production was determined by H2DCF-DA and MitoSOX Red probes with flow cytometry. NADPH oxidase activity and NOX2 protein levels were measured by lucigenin chemiluminescence and western blot. Results showed that lncRNA-ROR expression was increased in I/R patients and in H/R treatment of H9c2 cells and HCM. Moreover, lncRNA-ROR significantly promoted H/R-induced myocardial injury via stimulating release of LDH, MDA, SOD, and GSH-PX. Furthermore, lncRNA-ROR decreased cell viability, increased apoptosis, and regulated expression of apoptosis-associated factors. Additionally, lncRNA-ROR increased phosphorylation of p38 and ERK1/2 expression and inhibition of p38/MAPK, and rescued lncRNA-ROR-induced cell injury in H9c2 cells and HCM. ROS production, NADPH oxidase activity, and NOX2 protein levels were promoted by lncRNA-ROR. These data suggested that lncRNA-ROR acted as a therapeutic agent for the treatment of myocardial I/R injury.


Subject(s)
Humans , Myocardial Ischemia/metabolism , Myocardial Reperfusion Injury/metabolism , RNA, Long Noncoding/metabolism , Apoptosis , Blotting, Western , Cell Survival , Glutathione Peroxidase/metabolism , Hydro-Lyases/metabolism , Malondialdehyde/metabolism , Myocardial Ischemia/genetics , Myocardial Reperfusion Injury/genetics , Myocytes, Cardiac , Real-Time Polymerase Chain Reaction , RNA, Long Noncoding/genetics , Signal Transduction , Superoxide Dismutase/metabolism , Transfection
8.
Biol. Res ; 51: 17, 2018. graf
Article in English | LILACS | ID: biblio-950903

ABSTRACT

BACKGROUND: Improper control on reactive oxygen species (ROS) elimination process and formation of free radicals causes tissue dysfunction. Pineal hormone melatonin is considered a potent regulator of such oxidative damage in different vertebrates. Aim of the current communication is to evaluate the levels of oxidative stress and ROS induced damage, and amelioration of oxidative status through melatonin induced activation of signaling pathways. Hepatocytes were isolated from adult Labeo rohita and exposed to H2O2 at three different doses (12.5, 25 and 50 µM) to observe peroxide induced damage in fish hepatocytes. Melatonin (25, 50 and 100 µg/ml) was administered against the highest dose of H2O2. Enzymatic and non-enzymatic antioxidants such as malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) was measured spectrophotometrically. Expression level of heat shock proteins (HSP70 and HSP90), HSPs-associated signaling molecules (Akt, ERK, cytosolic and nuclear NFkB), and melatonin receptor was also measured by western blotting analysis. RESULTS: H2O2 induced oxidative stress significantly altered (P < 0.05) MDA and GSH level, SOD and CAT activity, and up regulated HSP70 and HSP90 expression in carp hepatocytes. Signaling proteins exhibited differential modulation as revealed from their expression patterns in H2O2-exposed fish hepatocytes, in comparison with control hepatocytes. Melatonin treatment of H2O2-stressed fish hepatocytes restored basal cellular oxidative status in a dose dependent manner. Melatonin was observed to be inducer of signaling process by modulation of signaling molecules and melatonin receptor. CONCLUSIONS: The results suggest that exogenous melatonin at the concentration of 100 µg/ml is required to improve oxidative status of the H2O2-stressed fish hepatocytes. In H2O2 exposed hepatocytes, melatonin modulates expression of HSP70 and HSP90 that enable the hepatocytes to become stress tolerant and survive by altering the actions of ERK, Akt, cytosolic and nuclear NFkB in the signal transduction pathways. Study also confirms that melatonin could act through melatonin receptor coupled to ERK/Akt signaling pathways. This understanding of the mechanism by which melatonin regulates oxidative status in the stressed hepatocytes may initiate the development of novel strategies for hepatic disease therapy in future.


Subject(s)
Animals , Signal Transduction/drug effects , Oxidative Stress/drug effects , Hepatocytes/drug effects , Hydrogen Peroxide/pharmacology , Melatonin/pharmacology , Spectrophotometry , Superoxide Dismutase/drug effects , Catalase/drug effects , Catalase/metabolism , Blotting, Western , NF-kappa B/drug effects , NF-kappa B/metabolism , Reactive Oxygen Species/metabolism , MAP Kinase Signaling System/drug effects , Hepatocytes/metabolism , Proto-Oncogene Proteins c-akt/drug effects , Fishes , Glutathione/drug effects , Glutathione/metabolism , Malondialdehyde/metabolism
9.
Rev. bras. anestesiol ; 67(1): 35-41, Jan.-Feb. 2017. tab, graf
Article in English | LILACS | ID: biblio-843351

ABSTRACT

Abstract Background and objectives: The aim of this study was to compare the effects of sevoflurane and propofol anesthesia on oxidative DNA damage that occurs in low-extremity ischemia and is caused by tourniquet application. Methods: Fourteen New Zealand rabbits were randomly allocated into two equal groups. Group S (n = 7) received sevoflurane (2.5-4 percent) inhalation and Group P (n = 7) received a propofol infusion (1-2 mg·kg-1·min-1), after which a pneumatic tourniquet was placed on the right lower extremity. Blood samples were collected prior to tourniquet placement (baseline), 120 min after ischemia, 15 min after ischemia and 120 minutes (min) after ischemia. Malondialdehyde (MDA) levels were analyzed to determine lipid peroxidation, and single cell gel electrophoresis (SCGE) was used to determine DNA damage. Results: At 15 min after ischemia, the MDA levels in Group P (8.15 ± 2.61 µM) were higher than baseline (6.26 ± 3.19 µM, p = 0.026) and Group S (4.98 ± 0.77 µM, p = 0.01). DNA damage was similar in both groups, although DNA damage was higher than baseline (tail moment 0.63 ± 0.27, tail intensity 3.76 ± 1.26) in Group P at the 15th minute of reperfusion (tail moment 1.05 ± 0.45, p = 0.06; tail intensity 5.33 ± 1.56, p = 0.01). The increase in tail moment and tail intensity returned to normal levels in both groups 2 hours after the termination of ischemia. Conclusion: Given that oxidative stress and genotoxic effect disappear in the late stages of reperfusion, we conclude that neither sevoflurane nor propofol can be considered superior to the other in anesthesia practices for extremity surgeries involving the use of a tourniquet.


Resumo Justificativa e objetivos: Comparar os efeitos da anestesia com sevoflurano e propofol sobre o dano oxidativo ao DNA que ocorre na isquemia de extremidade inferior e é causada pela aplicação de torniquete. Métodos: Foram alocados aleatoriamente em dois grupos iguais 14 coelhos da raça Nova Zelândia. Grupo S (n = 7) recebeu inalação de sevoflurano (2,5-4%) e Grupo P (n = 7) recebeu perfusão de propofol (1-2 mg·kg-1·min-1), logo após um torniquete pneumático foi colocado na extremidade inferior direita. Amostras de sangue foram coletadas antes da colocação do torniquete (fase basal), após 120 minutos de isquemia, 15 minutos após a isquemia e 120 minutos após a isquemia. Os níveis de malondialdeído (MDA) foram analisados para determinar a peroxidação de lipídios e eletroforese em gel de célula única (EGCU) foi usada para determinar o dano ao DNA. Resultados: Aos 15 minutos após a isquemia, os níveis de MDA no Grupo P (8,15 ± 2,61 µM) foram superiores aos da fase basal (6,26 ± 3,19 µM, p = 0,026) e dp Grupo S (4,98 ± 0,77 µM, p = 0,01). O dano causado ao DNA foi semelhante nos dois grupos, embora tenha sido maior do que na fase basal (momento da cauda 0,63 ± 0,27, intensidade da cauda 3,76 ± 1,26) no Grupo P no 15 minutos de reperfusão (momento da cauda 1,05 ± 0,45, p = 0,06; intensidade da cauda 5,33 ± 1,56, p = 0,01). O aumento no momento da cauda e a intensidade da cauda voltaram aos níveis normais nos dois grupos duas horas após o término da isquemia. Conclusão: Como o estresse oxidativo e o efeito genotóxico desaparecem nos estágios finais da reperfusão, concluímos que não há superioridade tanto de sevoflurano quanto de propofol em práticas de anestesia para procedimentos cirúrgicos de extremidades que envolvem o uso de torniquete.


Subject(s)
Animals , DNA Damage/drug effects , Propofol/pharmacology , Anesthetics, Intravenous/pharmacology , Anesthetics, Inhalation/pharmacology , Methyl Ethers/pharmacology , Rabbits , Tourniquets/adverse effects , Reperfusion Injury , Random Allocation , Acute Disease , Oxidative Stress/drug effects , Comet Assay , Sevoflurane , Malondialdehyde/metabolism
10.
Acta cir. bras ; 31(12): 813-820, Dec. 2016. graf
Article in English | LILACS | ID: biblio-837660

ABSTRACT

ABSTRACT PURPOSE: To evaluate the role of low molecular chitosan containing sepia ink (LMCS) in ethanol-induced (5 ml/kg) gastric ulcer in rats. METHODS: Animals were divided into four groups (n = 12): normal group (Normal), negative control group (Con), experiment group (LMCS) and positive control Omeprazole group (OMZ). Gastric empty rate was detected in the first 7 days. Rats were sacrificed at 7, 14 and 21 day for histology and ELISA detections. RESULTS: Gastric empty was no significant differences among the groups (P > 0.05). Histological observation showed gastric mucosal LMCS treated had better healing effect. Hydroxyproline (Hyp) was significantly increased from 7 day (P < 0.05). LMCS significantly inhibited malondialdehyde (MDA) generation for lipid peroxidation from 7 day (P < 0.05). LMCS significantly promoted the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) at the earlier stage (P < 0.05). OMZ had the similar effects above. As for myeloperoxidase (MPO), LMCS significantly decreased and restored it to normal levels from 7 day (P < 0.05), it is earlier than OMZ which is from 14 day. CONCLUSION: LMCS can improve gastric mucosa tissue repair, exert significant influences on oxidative and antioxidant enzyme activities and neutrophil infiltration.


Subject(s)
Animals , Rats , Stomach Ulcer/drug therapy , Chitosan/therapeutic use , Sepia/chemistry , Gastric Mucosa/drug effects , Anti-Ulcer Agents/therapeutic use , Antioxidants/pharmacology , Stomach Ulcer/chemically induced , Random Allocation , Chitosan/chemistry , Disease Models, Animal , Ethanol , Gastric Mucosa/pathology , Hydroxyproline/metabolism , Ink , Malondialdehyde/metabolism , Molecular Weight , Antioxidants/metabolism
11.
Acta cir. bras ; 31(6): 411-416, tab, graf
Article in English | LILACS | ID: lil-785016

ABSTRACT

ABSTRACT PURPOSE: To investigate the protective effect of metformin on testicular ischemia/reperfusion (I/R) injury in rats. METHODS: Eighteen adult male Wistar rats were randomly divided into three experimental groups (n=6), as follows: Sham, I/R, and Metformin. 1-hour ischemia was induced by the left testicular artery and vein clipping followed by 7 days of reperfusion. Metformin (100 mg/kg) was administrated orally for 7 days via oral gavage after ischemic period. At the end of trial, the left testis was removed for histological analysis and oxidative stress measurement. RESULTS: I/R reduced superoxide dismutase (SOD) activities and testicular Johnsen's scores accompanied by an elevation in malondialdehyde (MDA) and myeloperoxidase (MPO) levels in comparison with the sham group (P < 0.05). Compared to I/R group, metformin restored testicular Johnsen's scores, SOD activity, MDA and MPO levels (P < 0.05). CONCLUSION: Metformin has a protective effect against I/R injury on the testis.


Subject(s)
Animals , Male , Testis/blood supply , Reperfusion Injury/prevention & control , Protective Agents/pharmacology , Metformin/pharmacology , Superoxide Dismutase/metabolism , Testis/metabolism , Reperfusion Injury/metabolism , Random Allocation , Rats, Wistar , Peroxidase/metabolism , Oxidative Stress/drug effects , Models, Animal , Malondialdehyde/metabolism
12.
Acta cir. bras ; 31(5): 333-337, May 2016. graf
Article in English | LILACS | ID: lil-783795

ABSTRACT

ABSTRACT PURPOSE: To evaluate the effects of an intraperitoneal solution of methylene blue (MB), lidocaine and pentoxyphylline (PTX) on intestinal ischemic and reperfusion injury METHODS: Superior mesenteric artery was isolated and clamped in 36 adult male Sprague Dawley rats. After 60 minutes, clamp was removed and a group received intraperitoneally UNITO solution (PTX 25mg/kg + lidocaine 5mg/kg + MB 2mg/kg), while the other group was treated with warm 0.9% NaCl solution. Rats were euthanized 45 min after drug administration. Lung and bowel were collected for histological evaluation (using Park's score) and determination of myeloperoxidase (MPO) and malondialdehyde (MDA) levels. RESULTS: Control samples showed lymphoplasmocytic infiltrate and crypt necrosis of villi. MPO and MDA measurements shown no differences between treated and control groups. CONCLUSION: The combination of lidocaine, methylene blue and pentoxyphylline administered intraperitoneally at the studied dose, did not decreased histological lesion scores and biochemical markers levels in intestinal ischemia/reperfusion injury.


Subject(s)
Animals , Male , Pentoxifylline/therapeutic use , Reperfusion Injury/drug therapy , Intestines/blood supply , Lidocaine/therapeutic use , Methylene Blue/therapeutic use , Anti-Inflammatory Agents/therapeutic use , Pentoxifylline/administration & dosage , Random Allocation , Peroxidase/metabolism , Models, Animal , Drug Combinations , Drug Synergism , Inflammation/prevention & control , Inflammation/drug therapy , Infusions, Parenteral , Intestines/enzymology , Lidocaine/administration & dosage , Lung/blood supply , Lung/metabolism , Malondialdehyde/metabolism , Methylene Blue/administration & dosage , Anti-Inflammatory Agents/administration & dosage
13.
Acta cir. bras ; 31(3): 168-175, Mar. 2016. graf
Article in English | LILACS | ID: lil-777089

ABSTRACT

ABSTRACT PURPOSE : To investigate the effects of thiamine pyrophosphate (TPP) against desflurane induced hepatotoxicity. METHODS : Thirty experimental animals were divided into groups as healthy (HG), desflurane control (DCG) , TPP and desflurane group (TDG). 20 mg/kg TPP was injected to intraperitoneally TDG. After one hour of TPP administration, desflurane was applied for two hours. After 24 hours, liver tissues of the animals killed with decapitation were removed. The oxidant/antioxidant levels and ALT, AST and LDH activities were measured. The histopathological examinations were performed in the liver tissues for all rats. RESULTS : Notwithstanding the levels of oxidants and liver enzymes were significantly increased (p<0.0001), antioxidant levels were significantly decreased in DCG (p<0.0001). On contrary to the antioxidant parameters were increased (p<0.05) the oxidant parameters and liver enzymes were decreased in TDG (p<0.0001). Whereas multiple prominent, congestion, hemorrhage and dilatation were observed in sinusoids and lymphocyte-rich inflammation results in the centrilobular and portal areas of liver tissue in DCG, these findings were observed less frequently in TDG. CONCLUSİON : Thiamine pyrophosphate prevented liver oxidative damage induced with desflurane and may be useful in prophylaxis of desflurane induced hepatotoxicity.


Subject(s)
Animals , Male , Thiamine Pyrophosphate/therapeutic use , Anesthetics, Inhalation/adverse effects , Protective Agents/pharmacology , Chemical and Drug Induced Liver Injury/prevention & control , Isoflurane/analogs & derivatives , Aspartate Aminotransferases/drug effects , Aspartate Aminotransferases/metabolism , Rats, Wistar , Peroxidase/drug effects , Oxidative Stress/drug effects , Alanine Transaminase/drug effects , Alanine Transaminase/metabolism , Chemical and Drug Induced Liver Injury/metabolism , Glutathione/drug effects , Glutathione/metabolism , Isoflurane , L-Lactate Dehydrogenase/drug effects , L-Lactate Dehydrogenase/metabolism , Liver/enzymology , Liver/pathology , Malondialdehyde/metabolism , Nitric Oxide/metabolism
14.
Braz. j. med. biol. res ; 49(10): e5310, 2016. graf
Article in English | LILACS | ID: biblio-951650

ABSTRACT

Although it is well known that physical training ameliorates brain oxidative function after injuries by enhancing the levels of neurotrophic factors and oxidative status, there is little evidence addressing the influence of exercise training itself on brain oxidative damage and data is conflicting. This study investigated the effect of well-established swimming training protocol on lipid peroxidation and components of antioxidant system in the rat brain. Male Wistar rats were randomized into trained (5 days/week, 8 weeks, 30 min; n=8) and non-trained (n=7) groups. Forty-eight hours after the last session of exercise, animals were euthanized and the brain was collected for oxidative stress analysis. Swimming training decreased thiobarbituric acid reactive substances (TBARS) levels (P<0.05) and increased the activity of the antioxidant enzyme superoxide dismutase (SOD) (P<0.05) with no effect on brain non-enzymatic total antioxidant capacity, estimated by FRAP (ferric-reducing antioxidant power) assay (P>0.05). Moreover, the swimming training promoted metabolic adaptations, such as increased maximal workload capacity (P<0.05) and maintenance of body weight. In this context, the reduced TBARS content and increased SOD antioxidant activity induced by 8 weeks of swimming training are key factors in promoting brain resistance. In conclusion, swimming training attenuated oxidative damage and increased enzymatic antioxidant but not non-enzymatic status in the rat brain.


Subject(s)
Animals , Male , Physical Conditioning, Animal/physiology , Swimming/physiology , Brain/metabolism , Oxidative Stress/physiology , Exercise Therapy/methods , Antioxidants/metabolism , Reference Values , Spectrophotometry , Superoxide Dismutase/analysis , Time Factors , Body Weight , Lipid Peroxidation/physiology , Random Allocation , Reproducibility of Results , Reactive Oxygen Species/metabolism , Malondialdehyde/analysis , Malondialdehyde/metabolism , Antioxidants/analysis
15.
Yonsei Medical Journal ; : 664-673, 2016.
Article in English | WPRIM | ID: wpr-21847

ABSTRACT

PURPOSE: Diabetic nephropathy is a serious complication of type 2 diabetes mellitus, and delaying the development of diabetic nephropathy in patients with diabetes mellitus is very important. In this study, we investigated inflammation, oxidative stress, and lipid metabolism to assess whether curcumin ameliorates diabetic nephropathy. MATERIALS AND METHODS: Animals were divided into three groups: Long-Evans-Tokushima-Otsuka rats for normal controls, Otsuka-Long-Evans-Tokushima Fatty (OLETF) rats for the diabetic group, and curcumin-treated (100 mg/kg/day) OLETF rats. We measured body and epididymal fat weights, and examined plasma glucose, adiponectin, and lipid profiles at 45 weeks. To confirm renal damage, we measured albumin-creatinine ratio, superoxide dismutase (SOD), and malondialdehyde (MDA) in urine samples. Glomerular basement membrane thickness and slit pore density were evaluated in the renal cortex tissue of rats. Furthermore, we conducted adenosine monophosphate-activated protein kinase (AMPK) signaling and oxidative stress-related nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling to investigate mechanisms of lipotoxicity in kidneys. RESULTS: Curcumin ameliorated albuminuria, pathophysiologic changes on the glomerulus, urinary MDA, and urinary SOD related with elevated Nrf2 signaling, as well as serum lipid-related index and ectopic lipid accumulation through activation of AMPK signaling. CONCLUSION: Collectively, these findings indicate that curcumin exerts renoprotective effects by inhibiting renal lipid accumulation and oxidative stress through AMPK and Nrf2 signaling pathway.


Subject(s)
Albuminuria , Animals , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Curcumin/pharmacology , Diabetes Mellitus, Type 2/metabolism , Diabetic Nephropathies/complications , Gene Expression/drug effects , Inflammation , Kidney/drug effects , Kidney Glomerulus/metabolism , Lipid Metabolism/drug effects , Male , Malondialdehyde/metabolism , Oxidative Stress/drug effects , Rats , Rats, Inbred OLETF , Rats, Long-Evans , Superoxide Dismutase/metabolism
16.
Article in English | WPRIM | ID: wpr-50645

ABSTRACT

PURPOSE: To compare oxidative stress status in the aqueous humor of highly myopic eyes and control eyes. METHODS: Aqueous humor samples were collected from 15 highly myopic eyes (high myopia group) and 23 cataractous eyes (control group) during cataract surgery. Central corneal thickness, corneal endothelial cell density, hexagonality of corneal endothelial cells, and cell area of corneal endothelial cells were measured using specular microscopy. Axial length was measured using ultrasound biometry. 8-Hydroxydeoxyguanosine (8-OHdG) and malondialdehyde levels were measured using enzyme-linked immunosorbent assay. RESULTS: 8-OHdG level was lower in the aqueous humor of myopic patients than in that of control group (p = 0.014) and was positively correlated with central corneal thickness and negatively correlated with axial length (r = 0.511, p = 0.02; r = -0.382, p < 0.001). There was no correlation between 8-OHdG level and corneal endothelial cell density, hexagonality, or cell area. Malondialdehyde level did not show any correlation with any parameters evaluated. CONCLUSIONS: 8-OHdG might be a sensitive biomarker for evaluating oxidative stress status in the eye. Oxidative stress level was lower in the aqueous humor of highly myopic eyes compared to that in control eyes, which indicates lower metabolic activity in these eyes.


Subject(s)
Aged , Aqueous Humor/metabolism , Deoxyguanosine/analogs & derivatives , Enzyme-Linked Immunosorbent Assay , Female , Humans , Male , Malondialdehyde/metabolism , Middle Aged , Myopia/metabolism , Oxidative Stress , Refraction, Ocular/physiology , Severity of Illness Index
17.
Clinics ; 70(5): 350-355, 05/2015. tab, graf
Article in English | LILACS | ID: lil-748270

ABSTRACT

OBJECTIVE: Sacrococcygeal pilonidal sinus is common in young men and may recur over time after surgery. We investigated whether a factor exists that can aid in the determination of the preferred technique between the early Limberg flap and Karydakis flap techniques for treating recurrent pilonidal sinus. MATERIALS AND METHODS: This prospective and randomized study enrolled 71 patients with recurrent pilonidal sinus in whom the Limberg flap or Karydakis flap techniques were applied for reconstruction after excision. Patients were divided into two groups as follows: 37 patients were treated with the Limberg flap technique and 34 patients were treated with the Karydakis flap technique. Fluid collection, wound infection, flap edema, hematoma, partial wound separation, return to daily activities, pain score, complete healing time, painless seating and patient satisfaction were compared between the groups. ClinicalTrial.gov: NCT02287935. RESULTS: The development rates of total fluid collection, wound infection, flap edema, hematoma, and partial wound separation were 9.8%, 16%, 7%, 15% and 4.2%, respectively; total flap necrosis was not observed in any patient (p<0.001). During the average follow-up of 28 months, no patients (0%) developed recurrent disease. The two groups differed with respect to early surgical complications (p<0.001). CONCLUSION: In this study, use of the Limberg flap was associated with lower complication rates, shorter length of hospital stay, early return to work, low pain score, high patient satisfaction and better complete healing duration. Therefore, we recommend the Limberg flap for treatment of recurrent pilonidal sinus. .


Subject(s)
Animals , Male , Rats , Aryldialkylphosphatase/genetics , Environmental Pollutants/toxicity , Gene Expression Regulation, Enzymologic/drug effects , Liver/drug effects , Polychlorinated Biphenyls/toxicity , Antioxidants/metabolism , Aryldialkylphosphatase/blood , Cholesterol, HDL/blood , Cholesterol, LDL/blood , Dose-Response Relationship, Drug , Lipid Peroxidation/drug effects , Liver/enzymology , Malondialdehyde/metabolism , Rats, Sprague-Dawley , Thiobarbituric Acid Reactive Substances/metabolism
18.
Biol. Res ; 48: 1-9, 2015. ilus, graf, tab
Article in English | LILACS | ID: biblio-950783

ABSTRACT

BACKGROUND: To evaluate the hepatoprotective potential and invitro cytotoxicity studies of whole plant methanol extract of Rumex vesicarius L. Methanol extract at a dose of 100 mg/kg bw and 200 mg/kg bw were assessed for its hepatoprotective potential against CCl4-induced hepatotoxicity by monitoring activity levels of SGOT (Serum glutamic oxaloacetic transaminase), SGPT (Serum glutamic pyruvic transaminase), ALP (Alkaline phosphatase), TP (Total protein), TB (Total bilirubin) and SOD (Superoxide dismutase), CAT (Catalase), MDA (Malondialdehyde). The cytotoxicity of the same extract on HepG2 cell lines were also assessed using MTT assay method at the concentration of 62.5, 125, 250, 500 µg/ml. RESULTS: Pretreatment of animals with whole plant methanol extracts of Rumex vesicarius L. significantly reduced the liver damage and the symptoms of liver injury by restoration of architecture of liver. The biochemical parameters in serum also improved in treated groups compared to the control and standard (silymarin) groups. Histopathological investigation further corroborated these biochemical observations. The cytotoxicity results indicated that the plant extract which were inhibitory to the proliferation of HepG2 cell line with IC50 value of 563.33 ± 0.8 Mg/ml were not cytotoxic and appears to be safe. CONCLUSIONS: Rumex vesicarius L. whole plant methanol extract exhibit hepatoprotective activity. However the cytotoxicity in HepG2 is inexplicable and warrants further study.


Subject(s)
Humans , Animals , Male , Rats , Plant Extracts/pharmacology , Cytotoxins/pharmacology , Rumex/chemistry , Cell Proliferation/drug effects , Chemical and Drug Induced Liver Injury/drug therapy , Phytotherapy/methods , Aspartate Aminotransferases/metabolism , Silymarin/pharmacology , Superoxide Dismutase/metabolism , Tetrazolium Salts , Bilirubin/metabolism , Carbon Tetrachloride , Catalase/metabolism , Anticarcinogenic Agents/pharmacology , Rats, Wistar , Alanine Transaminase/metabolism , Methanol , Drinking/drug effects , Eating/drug effects , Alkaline Phosphatase/metabolism , Hep G2 Cells , Chemical and Drug Induced Liver Injury/metabolism , Chemical and Drug Induced Liver Injury/pathology , Formazans , Liver/drug effects , Liver/metabolism , Malondialdehyde/metabolism , Antioxidants/metabolism , Antioxidants/pharmacology
19.
Article in English | WPRIM | ID: wpr-206918

ABSTRACT

In the present study, we investigated the effects of treadmill exercise on lipid peroxidation and Cu,Zn-superoxide dismutase (SOD1) levels in the hippocampus of Zucker diabetic fatty (ZDF) rats and lean control rats (ZLC) during the onset of diabetes. At 7 weeks of age, ZLC and ZDF rats were either placed on a stationary treadmill or made to run for 1 h/day for 5 consecutive days at 16~22 m/min for 5 weeks. At 12 weeks of age, the ZDF rats had significantly higher blood glucose levels and body weight than the ZLC rats. In addition, malondialdehyde (MDA) levels in the hippocampus of the ZDF rats were significantly higher than those of the ZLC rats whereas SOD1 levels in the hippocampus of the ZDF rats were moderately decreased. Notably, treadmill exercise prevented the increase of blood glucose levels in ZDF rats. In addition, treadmill exercise significantly ameliorated changes in MDA and SOD1 levels in the hippocampus although SOD activity was not altered. These findings suggest that diabetes increases lipid peroxidation and decreases SOD1 levels, and treadmill exercise can mitigate diabetes-induced oxidative damage in the hippocampus.


Subject(s)
Animals , Diabetes Mellitus/enzymology , Female , Gene Expression Regulation, Enzymologic , Genotype , Hippocampus/enzymology , Lipid Peroxidation/physiology , Male , Malondialdehyde/metabolism , Physical Conditioning, Animal/physiology , Rats , Rats, Zucker , Superoxide Dismutase/genetics
20.
Acta cir. bras ; 29(12): 787-793, 12/2014. tab, graf
Article in English | LILACS | ID: lil-731031

ABSTRACT

PURPOSE: To study the anti-inflammatory actions of electroacupuncture (EAc) on an experimental colitis model in mice. METHODS: Thirty-eight male Swiss mice, divided in five groups, were subjected to induction of colitis by TNBS in 50% ethanol. Saline (SAL) and ethanol (ETNL) groups served as controls. TNBS+EAc and TNBS+ dexamethasone subgroups were treated with EAc 100Hz and dexamethasone (DEXA) 1 mg/Kg/day, respectively. After three days, a colon segment was obtained for quantification of myeloperoxidase (MPO) activity, immunohistochemistry for iNOS, malondialdehyde (MDA) and cytokines (IL-1β and IL-10). RESULTS: Neutrophilic activity, assayed as MPO activity, was significantly higher in the TNBS colitis group than that in the saline control group. TNBS+EAc group showed suppression of IL-10 in the colon. EAc treatment significantly reduced the concentration of MDA and the expression of iNOS, as compared to the other groups. CONCLUSION: Electroacupuncture 100Hz applied to acupoint ST-36 promotes an anti-inflammatory action on the TNBS-induced colitis, mediated by increase of IL-10 and decrease of iNOS expression. .


Subject(s)
Animals , Male , Mice , Anti-Inflammatory Agents/therapeutic use , Colitis/therapy , Electroacupuncture/methods , /metabolism , Nitric Oxide Synthase Type II/metabolism , Peroxidase/metabolism , Acupuncture Points , Colitis/chemically induced , Colon/metabolism , Disease Models, Animal , Immunohistochemistry , Inflammatory Bowel Diseases/drug therapy , Inflammatory Bowel Diseases/therapy , Interleukin-1beta/metabolism , Malondialdehyde/metabolism , Nitric Oxide Synthase Type II/antagonists & inhibitors , Random Allocation , Trinitrobenzenesulfonic Acid
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