姜黄素调控p38MAPK通路改善糖尿病心肌病的机制研究

The Protective Effect of Curcuminon Diabetic Cardiomyopathy by p38MAPK Pathway

目的探讨姜黄素(Cur)通过调控p38MAPK通路抑制炎症反应改善糖尿病心肌病的作用机制。方法50只雄性SPF级C57BL/6小鼠,随机选取20只作为正常组,剩余30只小鼠给予高糖、高脂饲料喂养4周后,连续5d腹腔注射50mg/(kg·d)链脲佐菌素,以空腹血糖≥11.1mol/L作为糖尿病造模成功标准。正常组小鼠随机分为正常对照组(Con组)和姜黄素对照组(Cur组),糖尿病小鼠随机分为糖尿病组(DM组)和姜黄素给药组(DM+Cur组)。实验结束后,ELISA法检测各组小鼠心肌组织匀浆液中炎症因子TNF-α和IL-6含量;免疫荧光法检测各组小鼠心肌组织中TNF-α水平;Western blot法检测各组小鼠心肌组织中p-p38、p38和MCP-1蛋白表达。结果Cur可明显逆转糖尿病所致小鼠心肌组织匀浆液中TNF-α和IL-6的变化,减少心肌组织中TNF-α的表达,下调糖尿病小鼠心肌组织中p38MAPK磷酸化水平和MCP-1蛋白的表达。结论姜黄素通过抑制炎症反应改善小鼠糖尿病心肌病,其作用机制可能与抑制p38MAPK信号转导通路有关。

Objective To investigate the effect of Curcumin(Cur)on myocardial tissue in diabetic mice by improving inflammation.Methods 50 male SPF C57BL/6 mice were randomly divided into normal control group(Con group),curcumin control group(Cur group),diabetes group(DM group)and curcumin administration group(DM+Cur group).The model of diabetes was established by intraperitoneal injection of streptozotocin at dose of 50 mg/(kg·d)for a consecutive 5 days after high sugar and high fat diet for 4 weeks.Fasting blood glucose≥11.1mmol/L was taken as the success criterion of diabetes modeling.The contents of TNF-αand IL-6 in myocardial tissue were detected by ELISA,the expression of TNF-αin myocardium of mice was measured by immunofluorescence staining,and the levels of p38MAPK,p-p38MAPK and MCP-1 protein in myocardium of mice were detected by Western blot.Results Curcumin significantly decreased the levels of TNF-αand IL-6 in diabetic mouse myocardial tissue,inhibited high glucose-induced phosphorylation of p38MAPK and the expression of MCP-1.Conclusion Curcumin has protective effect on myocardial tissue in diabetic mice by improving inflammation and the mechanisms maybe involved in the regulation of p38MAPK signaling pathway.