[6]-Gingerol isolated from ginger attenuates sodium arsenite induced oxidative stress and plays a corrective role in improving insulin signaling in mice

详细信息	查看全文 | 推荐本文 |

• 作者：Debrup Chakraborty ; Avinaba Mukherjee ; Sourav Sikdar ; Avijit Paul ; Samrat Ghosh ; Anisur Rahman Khuda-Bukhsh ; ^{khudabukhsh_48@rediffmail.com} ; ^{prof_arkb@yahoo.co.in}
• 关键词：Sodium arsenite ; [6]-Gingerol ; Oxidative stress ; Hyperglycemia ; GLUT4 ; Insulin signaling
• 刊名：Toxicology Letters
• 出版年：2012
• 期刊代码：49_03784274
• 类别：pha
• 出版时间：5 April, 2012
• 卷：210
• 期：1
• 页码：34-43
• 文件大小：1121 K

摘要

Arsenic toxicity induces type 2 diabetes via stress mediated pathway. In this study, we attempt to reveal how sodium arsenite (iAs) could induce stress mediated impaired insulin signaling in mice and if an isolated active fraction of ginger, [6]-gingerol could attenuate the iAs intoxicated hyperglycemic condition of mice and bring about improvement in their impaired insulin signaling. [6]-Gingerol treatment reduced elevated blood glucose level and oxidative stress by enhancing activity of super oxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and GSH. [6]-Gingerol also helped in increasing plasma insulin level, brought down after iAs exposure. iAs treatment to primary cell culture of 尾-cells and hepatocytes in vitro produced cyto-degenerative effect and accumulated reactive oxygen species (ROS) in pancreatic 尾-cells and hepatocytes of mice. [6]-Gingerol appeared to inhibit/intervene iAs induced cyto-degeneration of pancreatic 尾-cells and hepatocytes, helped in scavenging the free radicals. The over-expression of TNF伪 and IL6 in iAs intoxicated mice was down-regulated by [6]-gingerol treatment. iAs intoxication reduced expression levels of GLUT4, IRS-1, IRS-2, PI3K, AKT, PPAR纬 signaling molecules; [6]-gingerol mediated its action through enhancing the expressions of these signaling molecules, both at protein and mRNA levels. Thus, our results suggest that [6]-gingerol possesses an anti-hyperglycemic property and can improve impaired insulin signaling in arsenic intoxicated mice.