Aloe-Emodin Protects RIN-5F (Pancreatic beta-cell) Cell from Glucotoxicity via Regulation of Pro-Inflammatory Cytokine and Downregulation of Bax and Caspase 3.
10.4062/biomolther.2015.056
- Author:
Ali A ALSHATWI
1
;
P SUBASH-BABU
Author Information
1. Adipogenesis and Immunobiology Research Lab, Department of Food Sciences and Nutrition, College of Food Sciences and Agriculture, King Saud University, Riyadh 11451, Kingdom of Saudi Arabia. subashbabu80@hotmail.com
- Publication Type:Original Article
- Keywords:
Aloe-emodin;
Glucotoxicity;
RIN-5F cells;
Apoptosis;
ROS
- MeSH:
Apoptosis;
Caspase 3*;
Cell Survival;
DNA Fragmentation;
Down-Regulation*;
Glucose;
Insulin
- From:Biomolecules & Therapeutics
2016;24(1):49-56
- CountryRepublic of Korea
- Language:English
-
Abstract:
To determine the protective effect of aloe-emodin (AE) from high glucose induced toxicity in RIN-5F (pancreatic beta-cell) cell and restoration of its function was analyzed. RIN-5F cells have been cultured in high glucose (25 mM glucose) condition, with and without AE treatment. RIN-5F cells cultured in high glucose decreased cell viability and increased ROS levels after 48 hr compared with standard medium (5.5 mM glucose). Glucotoxicity was confirmed by significantly increased ROS production, increased pro-inflammatory (IFN-gamma, IL-1beta,) & decreased anti-inflammatory (IL-6&IL-10) cytokine levels, increased DNA fragmentation. In addition, we found increased Bax, caspase 3, Fadd, and Fas and significantly reduced Bcl-2 expression after 48 hr. RIN-5F treated with both high glucose and AE (20 muM) decreased ROS generation and prevent RIN-5F cell from glucotoxicity. In addition, AE treated cells cultured in high glucose were transferred to standard medium, normal responsiveness to glucose was restored within 8hr and normal basal insulin release within 24 hr was achieved when compared to high glucose.
