生脉散对2型糖尿病性心肌病大鼠心肌的保护作用

Effect of Shengmai San on the on the Rats of Diabetic Cardiomyopathy

目的:探讨生脉散对糖尿病性心肌病(DCM)大鼠的保护作用。方法:SD大鼠42只,采用高脂高热量饮食诱导出胰岛素抵抗,加单次中等剂量(50mg/kg)腹腔注射链脲佐菌素建立DCM动物模型,12周后采用心电图评价心肌受损情况,取血检测血糖、胆固醇、甘油三酯,Masson染色检测左室心肌胶原含量,Tunel凋亡试剂盒检测心肌细胞凋亡程度,电镜观察心肌亚细胞结构破坏程度,同时采用免疫组织化学染色检测TSP-1、TGF-β1、Chymase和TRB-3蛋白的表达水平,采用Westernblotting技术检测TSP-1、A-TGFβ1和L-TGF-β1蛋白的表达水平变化。实时荧光定量PCR检测TSP-1和TRB-3mRNA表达水平的变化。结果:与模型组相比,生脉散组大鼠血糖、胆固醇、甘油三酯明显降低,心肌组织破坏程度较轻,胶原纤维含量显著减少,电镜观察心肌细胞亚细胞结构破坏程度较轻,免疫组化心肌TSP-1、TGF-β1以及TRB-3的表达水平、Western心肌tsp-1、A-TGFβ1和L-TGF-β1蛋白表达水平、PCR、TSP-1mRNA和TRB-3mRNA表达水平降低。结论:生脉散可通过多条途径抑制糖尿病心肌病大鼠的心肌纤维化,显著延缓糖尿病心肌病的发生进程。

Objective：Observe the effect of Shengmai San on the diabetic cardiomyopathy（DCM）.Methods：The rat model of DCM was established by eating a high-fat diet together with injection of high dose streptozotocin（50mg/kg） intraperitoneally.After 12 weeks,electrocardiogram was used to evaluate the damage of the myocardial,blood serum GLU,cholesterin and TG were tested by Clinical Chemistry Test Systems.The content of collagen was quantified by Masson staining.Level of cardiomyocyte apoptosis tested by Tunel apoptosis kit.The mRNA level of TSP-1 and TRB-3 was determined by quantification real time RT-PCR,while the protein level of TSP-1、A-TGF-β1 and L-TGF-β1 was analyzed by Western blotting and the protein level of TSP-1、TGF-β1、TRB-3 and Chymase was analyzed by immunohistochemistry.Results：Compared with control group,the rats blood glucose,cholesterol,triglycerides of Shengmai San group were significantly decreased.The Myocardial tissue was less damaged and the collagen content was less than control group.The expression of tsp-1,A-TGF-1 and L-TGF-β1 of the mixed liquor of Shengmai San and Danshen Decoction group in the diabetic cardiac muscle were much less than that in control group.The mRNA level of tsp-1 and TRB-3 were lower than control group by PCR detection.Conclusion：Shengmai San can inhibit the process of fibrosis in diabetic cardiomyopathy myocardial rats muscle and delay the formation of diabetic cardiomyopathy through of hyperglycemia rats through many signal pathways.