姜黄素衍生物B06对2型糖尿病大鼠心肌的保护作用及其机制探讨

The effect and mechanism of curcumin derivative B06 on the myocardium from type 2 diabetic rats

目的:研究姜黄素衍生物B06对2型糖尿病大鼠心肌的保护作用及机制。方法:雄性SD大鼠35只,随机均分为正常对照组(NC组)、高脂组(HF组)、高脂治疗组(FT组)、糖尿病组(DM组)和糖尿病治疗组(DT组)(n=7),后四组高脂喂养4周后,DM组及DT组用低剂量链脲佐菌素(STZ)诱导糖尿病,FT组和DT组用0.2 mg/kg·d的姜黄素衍生物B06灌胃。用生化方法测大鼠血糖和血脂浓度,用ELISA法测血胰岛素水平,并计算胰岛素抵抗指数,用光镜和电镜观察心肌形态,用Western blot法测心肌腺苷酸活化蛋白激酶ê(AMPKê)和磷酸化腺苷酸活化蛋白激酶ê(p-AMPKê)的蛋白表达。结果:HF组及DM组血糖、血脂、血胰岛素、胰岛素抵抗指数升高,经B06治疗后均下降;HF组及DM组AMPKê和p-AMPKê表达下降,经B06治疗后升高;DM组心肌间质胶原纤维增多,心肌细胞内线粒体扩张,经B06治疗后病变减轻。结论:B06可缓解2型糖尿病大鼠心肌病变,AMPKê和p-AMPKê表达升高可能参与其中。

Objective： To investigate the protective effect and mechanism of curcumin derivatives B06 on myocardium from type 2 diabetic rats. Methods：Thirty-five male SD rats were randomly divided into 5 groups, normal control group（NC group）, high fat group（HF group）, high fat treatment group（FY group）, diabetes mellitus group（DM group） and diabetes treatment group（DT group） （ n = 7）. The late four groups were fed with high fat food, after four weeks of high fat feeding, the rats from DM group and DT group were injected with low dosage of septozocin intraperitoneally to induce diabetes mellitus, FF group and DT group were gavaged with curcumin derivatives B06 at the dosage of 0.2 mg/kg d. The blood glucose and lipid were detected biochemically, blood insulin was assayed by ELISA and the insulin resistance index was calc^ated, the morphology of myocardium was observed by light and transmission electron microscopy, the protein expression of AMP-acti- vated protein kinase a（AMPKa） and phosphorylated AMP-activated protein kinase u（p-A_MPKct） in myecardium were tested by Western blot. Results：The level of blood glucose, lipid, insulin and the insulin resistance index were increased in HF group and DM group, but they were decreased after the treatment with B06. The expression of AMPKct and p-AMPKct were decreased, but they became increased after the treat- ment of B06. There were increased collagen frbers in interstitium and expansion of mitochondria in cytoplasm of myecardium from DM group, but they were ameliorated in B06 treatment group. Conclusion： It is suggested that B06 may relieve the damage of myecardium from type 2 di- abetic rats and the increased expression of AMPKn and p-AMPKct may be involved in it.