Protection of INS-1 Cells from Free Fatty Acid-induced Apoptosis by Inhibiting the Glycogen Synthase

• 作 者: WU Wei LUO Xiaoping
• 机 构: Department of Pediatrics, Tongl Hospital, Tongji Medical College, Huazhong University of Science and
• 出 处: 华中科技大学学报（医学）（英德文版）
• 发表日期: 2007年5期
• 关键词: glycogen synthase kinase 3 apoptosis oleic acid

To examine the role of glycogen synthase kinase 3 (GSK-3) in the apoptosis of pancreatic β-cells to better understand the pathogenesis and to find new approach to the treatment of type 2 dia-betes, apoptosis was induced by oleic acid (OA) in INS-1 cells and the activity of GSK-3 was inhib-ited by LiCl. The PI staining and flow cytometry were employed for the evaluation of apoptosis. The phosphorylation level of GSK-3 was detected by West 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 apop-tosis 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 β-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.