红景天苷对糖尿病心肌病MAPK信号通路作用机制

Effect Mechanism of Salidroside on MAPK Signaling Pathway in Diabetic Cardiomyopathy

目的探讨红景天苷对链脲佐菌素诱导的糖尿病心肌病(DCM)大鼠丝裂原活化蛋白激酶(MAPK)信号通路的影响,并分析可能的作用机制。方法将SD大鼠随机分为空白组、模型组、红景天苷低剂量组(25 mg/kg)、红景天苷中剂量组(50 mg/kg)、红景天苷高剂量组(100 mg/kg)。灌胃给药12周,采用Western Blot法测定心脏组织中细胞外信号调节激酶(ERK)、c-Jun氨基末端激酶(JNK)以及p38丝裂原活化蛋白激酶(p38MAPK)的表达情况;荧光定量PCR法测定c-jun、c-fos mRNA的相对表达量;HE染色光镜检查心脏组织病理切片。结果研究发现DCM大鼠心脏组织c-fosmRNA、c-jun mRNA、JNK、ERK及p38 MAPK蛋白表达明显上调,红景天苷可显著抑制上述指标表达上调,并减轻DCM大鼠心脏组织病变。结论红景天苷通过抑制DCM大鼠MAPK信号通路而减轻其心肌纤维化损伤。

Objective To explore the impacts of salidroside on MAPK signaling pathway in diabetic cardiomyopathy( DCM) induced by streptozotocin and analyze its potential mechanism. Methods SD rats were randomized into a blank group,a model group,a low-dose salidroside( 25 mg / kg) group,a moderate-dose salidroside( 50 mg / kg) and a high-dose salidroside( 100 mg / kg) group. In 12 weeks after lavage,the western blot method was used to determine the expressions of ERK,c-Jun JNK and p38 MAPK in cardiac tissue. The fluorescence quantitative PCR method was used to determine the relative expressions of c-jun and c-fos mRNA. HE staining ligth microscope was used for the examination of pathological slice of cardiac tissue. Results The research discovered that the protein expressions of c-fos mRNA,c-jun mRNA,JNK,ERK and p38 MAPK were apparently up-regulated in cardiac tissue. Salidroside inhibited significantly the up-regulation of the above-mention indicators and alleviated the pathological changes of cardiac tissue in DCM rats. Conclusion Salidroside alleviates the damages of myocardiac fibrosis via the inhibition of MAPK signal pathway in the rats.