姜黄素缓解糖尿病小鼠脑组织氧化损伤的机制研究

Mechanisms of Curcumin to Alleviate Oxidative Damage in the Brain Tissue of Diabetic Mice

目的探讨姜黄素(Cur)对糖尿病(DM)小鼠脑组织氧化损伤的改善情况。方法高脂喂养联合STZ腹腔注射构建小鼠DM模型,治疗组小鼠灌胃给予姜黄素。试剂盒检测小鼠脑组织中SOD活力和MDA含量;Western blot法检测小鼠脑组织中p-AKT/AKT、p-AMPK/AMPK、p-GSK3β/GSK3β、p-TAU/TAU蛋白的表达。结果与DM组相比,Cur治疗组小鼠脑组织中SOD显著上调(P<0.01),MDA含量显著下调。AKT、AMPK、GSK-3β蛋白表达水平没有显著变化,p-AKT、p-AMPK、p-GSK3β蛋白表达水平均上调,显示AKT/AMPK/GSK3β通路被激活。Cur治疗后,p-TAU蛋白表达降低。结论Cur可能通过AKT/AMPK/GSK3β通路缓解DM小鼠脑组织的氧化损伤,降低TAU蛋白磷酸化水平。

Objective To investigate the effect of curcumin(Cur)on oxidative damage of brain tissue in diabetic(DM)mice.Methods The mice model of DM was established by high fat feeding combined with intraperitoneal injection of streptozotocin(STZ).The mice in the treatment group were given Cur by intragastric administration.SOD activity and MDA content in brain tissue of mice were detected by kit.The expression of p-AKT/AKT,p-AMPK/AMPK,p-GSK3β/GSK3βand p-TAU/TAU proteins in mouse brain tissue were detected by Western blot.Results Compared with DM group,SOD was significantly up-regulated and MDA was significantly down-regulated in Cur group(P<0.01).The expression levels of AKT,AMPK,GSK3βhad no significant change,while p-AKT,p-AMPK and p-GSK3βin the Cur treatment group were up-regulated,indicating that the AKT/AMPK/GSK3βpathway was activated.After Cur treatment,p-TAU protein expression decreased.Conclusion Cur may alleviate oxidative damage and decrease TAU phosphorylation in brain tissue of DM mice through AKT/AMPK/GSK3βpathway.