Protection of INS-1 cells from free fatty acid-induced apoptosis by inhibiting the glycogen synthase kinase-3.
- Author:
Wei, WU
;
Xiaoping, LUO
- Publication Type:Journal Article
- MeSH:
Apoptosis/*drug effects;
Cell Line;
Fatty Acids, Nonesterified/*pharmacology;
Glycogen Synthase Kinase 3/*metabolism;
Insulin-Secreting Cells/*cytology;
Oleic Acid/pharmacology;
Phosphorylation
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2007;27(5):483-6
- CountryChina
- Language:English
-
Abstract:
To examine the role of glycogen synthase kinase 3 (GSK-3) in the apoptosis of pancreatic beta-cells to better understand the pathogenesis and to find new approach to the treatment of type 2 diabetes, apoptosis was induced by oleic acid (OA) in INS-1 cells and the activity of GSK-3 was inhibited by LiCl. The PI staining and flow cytometry were employed for the evaluation of apoptosis. The phosphorylation level of GSK-3 was detected by Western blotting. The results showed that OA at 0.4 mmol/L could cause conspicuous apoptosis of INS-1 cells and the activity of GSK-3 was significantly increased. After the treatment with 24 mmol/L of LiCl, a inhibitor of GSK-3, the OA-induced apoptosis of INS-1 cells was lessened and the phosphorylation of GSK-3 was increased remarkably. It is concluded that GSK-3 activation plays an important role in OA-induced apoptosis in pancreatic beta-cells and inhibition of the GSK-3 activity can effectively protect INS-1 cells from the OA-induced apoptosis. Our study provides a new experimental basis and target for the clinical treatment of type-2 diabetes.