Protection of beta-pancreatic cells from dysfunctionality of insulin using vitexin by apoptosis of INS-1 cells

Aims This study was performed to explore the possible beneficial effects of vitexin on high glucose (HG)-induced cytotoxicity in pancreatic beta-cells. Methods INS-1 pancreatic beta-cell line has used this study. HG-induced (33 Mm) exposed INS-1 cell death; the apoptosis INS-1 cells treated vitexin 10, 20, 40, and 80 mu g/mL for 24 hours. The anti-apoptosis properties were evaluated by MTT assay, glucose-stimulated insulin secretion assay, biochemical assay, annexin-V-FITC staining and western blot analysis. Results These findings demonstrate that vitexin treatment improved the HG-exposure, reduced the INS-1 cell viability and significantly enhanced glucose-stimulated insulin secretion in a dose-dependent manner. The antioxidant studies revealed that vitexin treatment significantly decreased lipid peroxidation and reactive oxygen species and increased antioxidant level of INS-1 cell line in 24 hrs. The findings of the study suggested that in the vitexin treatment group, pancreatic apoptosis and Bax protein expression reduced significantly. At the same time, Bcl-2 protein expression increased, and NF-kappa B protein in HG-induced INS-cells was inhibited. Conclusion Therefore, our results suggest that vitexin can be successfully used to regulate the expression of Bcl-2 family proteins, reduce lipid peroxidation and to improve the secretion of antioxidants in pancreatic beta-cell lines.