Protection of pancreatic beta cells against high glucose-induced toxicity by astaxanthin-s-allyl cysteine diester: alteration of oxidative stress and apoptotic-related protein expression

Abstract

Purpose: High glucose (HG)-induced oxidative stress is associated with apoptosis in pancreatic β-cells. The protective effect of astaxanthin-s-allyl cysteine diester (AST-SAC) against HG-induced oxidative stress in pancreatic β-cells (βTC-tet cell line) in in vitro was studied.

Materials and Methods: βTC-tet cell line was exposed to HG in the presence and absence of AST-SAC. Various parameters such as cell viability, reactive oxygen species generation, mitochondrial membrane potential, DNA fragmentation and expression of proteins involved in apoptosis [p53, B-cell lymphoma 2 (Bcl-2), Bcl-2 associated X (Bax), cytochrome c and caspase 3] were studied.

Results: Pre-treatment of βTC-tet cells with AST-SAC (4, 8 and 12 μg/ml) in the presence of HG (25 mM) protected the viability of the cells in a dose-dependent manner. AST-SAC treatment mitigated the oxidative stress thereby preventing the mitochondrial dysfunction, DNA damage and apoptosis in βTC-tet cells against HG toxicity. Treatment with AST-SAC prevented the increased expression of p53 under HG conditions. Further, AST-SAC treatment maintained the level of pro-apoptotic (Bax, cleaved caspase-3 and cytochrome c) and anti-apoptotic (Bcl-2) proteins to that of the control level under HG exposed conditions in βTC-tet cells.

Conclusion: Altogether, AST-SAC alleviated HG-induced oxidative damage and apoptosis in pancreatic β-cells by enhancing the antioxidant status and altering apoptotic-related protein expression.

Keywords:

• Astaxanthin-s-allyl cysteine diester
• pancreatic β-cells
• apoptosis
• high glucose
• oxidative stress

Acknowledgement

Dr. S. Penislusshiyan acknowledges Human Resource Development, Department of Health Research, Ministry of Health and Family Welfare, India for the award of a young scientist fellowship (Ref. No. R0.12014/51/2020-HR). Dr. L. Chitra acknowledges the University Grants Commission, India for the award of Dr. D.S. Kothari Postdoctoral Fellowship (Ref. No. F0.4–2/2006 (BSR)/BL/17–18/0313).

Disclosure statement

All authors declare no conflict of interest.

Data availability statement

The Data that support the findings of this study are available from the corresponding author (TP), upon reasonable request.

Additional information

Funding

The research is funded by Human Resource Development, Department of Health Research, Ministry of Health and Family Welfare, India under young scientist scheme.