雷公藤多苷对实验性糖尿病心肌病大鼠的影响

目的:探讨雷公藤多苷对实验性糖尿病心肌病大鼠的心脏保护作用.方法:用链脲佐菌素(STZ将sD大鼠造模成糖尿病心肌病模型,分为雷公藤多苷组,模型组,另设正常组(均n=8).雷公藤多苷组给予雷公藤多苷(18 mg·kg~(-1)),其余各组给以等量生理盐水,持续给药3个月.给药结束后测血糖、心功能、心脏指数,用免疫组化法观察心肌核因子-κB(NF-κB和细胞间黏附分子-1(ICAM-1)表达,同时用电子显微镜观察大鼠心肌超微结构变化.结果:与模型组比较,雷公藤多苷能减小心脏指数,保护心功能,抑制NF-KB和ICAM-1表达;明显延缓心肌细胞线粒体、心肌纤维细胞的病理改变.结论:雷公藤多苷具有保护糖尿病心肌病大鼠心脏作用,其机制可能与抑制炎症反应和免疫抑制作用有关.

Effect of tripterysium glucosides on diabetic cardiomyopathy in rats

Objective: To observe the effect of heart protection on diabetic cardiomyopathy in rats by tripterysium glucosides.  Method: The rat diabetic cardiomyopathy rats model are made by streptozotocin, then divided into tripterysium glucosides group (n=8) and model group (n=8). In addition, the control group is established (n=8). Glucosides group was orally administrated tripterysium glucosides (18 mg·kg-1), the control groups was orally administrated same volume NS for 3 months. Blood sugar, heart function and cardiac index were detected after 3 months. Immunohistochemical techniques were used to detect NF κB and ICAM 1 expression. Ultrastructure of cardiac muscle cell were observed by electronmicroscope.  Result: Compared with model group, cardiac index was decreased after tripterysium glucosides administration, and LVSP, LVEDP, +dp/dtmax, -dp/dtmax,  were improved, and the expression of nuclear Factor κB (NF κB) and intercellular adhension molecule 1  (ICAM 1) was inhibited. Ultrastructure of cardiac muscle cell such as mitochondrion and cardiac muscle fibers was atttenuated.  Conclusion: Tripterysium glucosides could protect rat diabetic cardiomyopathy rats' heart. These function may be related to inflammatory reaction inhibition and immunosuppression of tripterysium glucosides.