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目的:研究穿心莲内酯(AP)对异丙肾上腺素(Iso)诱导大鼠心肌肥厚模型丝分裂原活化蛋白激酶(MAPK)的影响。方法:大鼠分为5组:对照组、心肌肥厚模型组、溶剂对照组、穿心莲内酯低剂量及高剂量组,采用连续10天背部皮下注射Iso建立心肌肥厚模型。连续给药14 d后,称量大鼠体重及全心、左心室重量,观察各指数变化。结果:与正常对照组比较,模型及溶剂组大鼠全心、左心室重量指数均增大,ERK磷酸化表达上升,p38磷酸化表达降低。给予穿心莲内酯后,与模型组比较,心肌肥厚模型大鼠全心、左心室重量指数下降,ERK磷酸化表达显著下降,p38磷酸化表达显著增多。结论:穿心莲内酯可以调控ERK、p38两条MAPK信号转导通路途径,延缓Iso诱导的大鼠心肌肥厚的作用。
AIM: To investigate the effects of andrographolide (AP) on mitogen - activated protein kinase (MAPK) induced by isoproterenol (ISO) in rat cardiac hypertrophy model. Methods: The rats were divided into 5 groups: control group, model group of cardiac hypertrophy, solvent control group, and andrographolide low dose and high dose group. The model of myocardial hypertrophy was established by subcutaneous injection of Iso for 10 days. After continuous administration for 14 days, the body weight and heart weight of the rats and the weight of the left ventricle were measured to observe the change of each index. Results: Compared with the normal control group, the whole heart and left ventricular weight index of model and solvent group increased, the phosphorylation of ERK increased and the expression of phosphorylated p38 decreased. After administration of andrographolide, compared with the model group, the cardiac and left ventricular mass index of rats with cardiac hypertrophy decreased, the phosphorylation of ERK significantly decreased, and the expression of p38 phosphorylation increased significantly. Conclusion: Andrographolide can regulate ERK, p38 two MAPK signal transduction pathway, delay Iso induced rat cardiac hypertrophy.