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

Arch Physiol Biochem. 2023 Oct;129(5):1160-1167. doi: 10.1080/13813455.2021.1910714. Epub 2021 Apr 9.

Abstract

Aims: This study was performed to explore the possible beneficial effects of vitexin on high glucose (HG)-induced cytotoxicity in pancreatic β-cells.

Methods: INS-1 pancreatic β-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 µg/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-κB 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 β-cell lines.

Keywords: NF-κB pancreatic β-cells; Vitexin; anti-apoptosis; antioxidant; high glucose; insulin secretion.

MeSH terms

  • Antioxidants / metabolism
  • Antioxidants / pharmacology
  • Cell Survival
  • Glucose / metabolism
  • Insulin* / metabolism
  • Insulin-Secreting Cells* / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism

Substances

  • Insulin
  • Antioxidants
  • vitexin
  • Proto-Oncogene Proteins c-bcl-2
  • Glucose