Protection of INS-1 cells from free fatty acid-induced apoptosis by inhibiting the glycogen synthase kinase-3.
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.
Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. wuweir11@163.com
Wei
W
Wu
Xiaoping
X
Luo
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002460:Cell Line; D005230:Fatty Acids, Nonesterified / Q000494:pharmacology*; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism*; D050417:Insulin-Secreting Cells / Q000166:cytology*; D019301:Oleic Acid / Q000494:pharmacology; D010766:Phosphorylation; D051381:Rats
D005230:Fatty Acids, Nonesterified; D019301:Oleic Acid; D038362:Glycogen Synthase Kinase 3