Protective effect of cyanidin-3-O-glucoside against tacrolimus-induced pancreatic beta cell dysfunction
- Affiliations
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- 1Division of Transplant Surgery, Department of Surgery, Gangneung Asan Hospital, Gangneung, Korea
- 2Department of Surgery, Gangneung Asan Hospital, Gangneung, Korea
Abstract
- Background
Tacrolimus (FK506) induces pancreatic cell dysfunction, causing new-onset diabetes mellitus (NODM) after transplantation. Cyanidin-3-O-glucoside (C3G), a major anthocyanin found in the extract of Chinese bayberry has powerful antioxidant capacity. Here, we investigated the protective role of C3G on FK506-induced pancreatic beta cell dysfunction.
Methods
In this study, INS-1 cell cultured with or without C3G were treated with FK506. The INS-1 cell were used, and treated with FK506 and C3G for 24-hour duration. INS-1 cell was assayed to determine C3G effect on cell viability and function, reactive oxygen species (ROS), oxidative stress, apoptosis, and the presence of inflammatory as well as autophagic markers.
Results
C3G treatment of INS-1 cell exposed to FK506 increased cell viability, beta cell secretory function and further alleviate cell apoptosis. A reduction in MDA and an increase in HO-1 gene expression as well as in vitro function were also observed in C3G-treated INS-1 cell exposed to FK506. Additionally, treatment with C3G resulted in a significant reduction in the gene expression of inflammatory markers IL-1 beta and TNF-a as well as an increase in LC3 autophagic marker in INS-1 cell treated with FK506.
Conclusions
C3G appears to have a protective effect on INS-1 cell against FK506 in vitro, possibly through its anti-oxidant property and alteration of inflammatory pathways.