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Mol Biol Rep ; 50(2): 1311-1320, 2023 Feb.
Article in English | MEDLINE | ID: mdl-36454432

ABSTRACT

BACKGROUND: Oxidative stress is known to impair cellular functions and, therefore, plays a significant role in the pathophysiology of various diseases, including diabetes. The persistently elevated glucose levels may cause enhanced mitochondrial reactive oxygen species generation, which in turn can damage the pancreatic ß-cells. In this study, we have investigated the effect of vanillic acid on preventing H2O2-induced ß-cells death and retaining its insulin secretion potentiating effect in the presence of H2O2. METHODS: The insulin secretion from the BRIN-BD11 cells was quantified using ELISA-based assays. The viability of the cells was assessed by estimated by the [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] (MTT) colorimetric assay and DAPI staining. The expression levels of apoptotic and antioxidant proteins were estimated by western blot experiments. RESULTS: Vanillic acid protected pancreatic ß-cells viability and function under the H2O2 oxidative stress condition. The Erk1/2 activation appears to play an important role in vanillic acid potentiated insulin secretion and protection of the ß-cells in the presence of H2O2. Vanillic acid pretreated cells exhibited enhanced expression of antioxidant enzymes such as catalase and SOD-2 and reduced the expression of proapoptotic markers such as BAX and BAD. In addition, it also enhanced the expression of oxidative stress-sensitive transcription factor Nrf-2 and cell survival protein Akt. CONCLUSION: The present study shows that vanillic acid potentiates insulin secretion and protects pancreatic ß-cells from H2O2-induced oxidative stress.


Subject(s)
Antioxidants , Insulin-Secreting Cells , Antioxidants/pharmacology , Antioxidants/metabolism , Insulin Secretion , Hydrogen Peroxide/toxicity , Hydrogen Peroxide/metabolism , Vanillic Acid/pharmacology , Apoptosis , Oxidative Stress , Reactive Oxygen Species/metabolism , Insulin-Secreting Cells/metabolism , Insulin/metabolism
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