【摘要】 目的:研究丹酚酸A对心肌梗死大鼠心肌纤维化及心功能的作用及其机制。方法:将24只SD大鼠随机分为假手术组、模型组和丹酚酸A组,每组8只。模型组和丹酚酸A组复制大鼠心肌梗死模型。比较3组大鼠的心功能,采用酶联免疫吸附试验(ELISA)法检测血清中肌钙蛋白T、CK-MB和NT-proBNP水平,Masson染色法观察心肌纤维化,计算心肌胶原容积分数(CVF),免疫组织化学染色检测Col-Ⅰ和Col-Ⅲ蛋白表达,Western blotting法检测心肌组织TGF-β1、Smad2及磷酸化(p-)Smad2蛋白表达。结果:与假手术组比较,模型组LVEDP、CVF和血清肌钙蛋白T、CK-MB和NT-proBNP水平明显升高,LVSP、+dp/dtmax和-dp/dtmax明显降低(P<0.05);与模型组比较,丹酚酸A组LVEDP、CVF和血清肌钙蛋白T、CK-MB和NT-proBNP水平明显降低,LVSP、+dp/dtmax和-dp/dtmax明显升高(P<0.05)。与模型组比较,丹酚酸A组Col-Ⅰ、Col-ⅢTGF-β1和pSmad2蛋白表达明显降低(P<0.05)。结论:丹酚酸A能够减轻心肌梗死大鼠心肌纤维化,改善心功能,可能与抑制TGF-β1/Smad2信号通路有关。更多还原

【Abstract】 Objective: To study the role and mechanism of salvianolic acid A on myocardial fibrosis and cardiac function in myocardial infarction rats. Methods: A total of 24 SD rats were randomly divided into sham-operation group, model group and salvianolic acid A group, with 8 rats in each group. Rat myocardial infarction models were established in the model group and salvianolic acid A group by ligation of the left anterior descending coronary artery. Cardiac function was compared. The levels of troponin T, CK-MB, and NT-proBNP in serum were detected by ELISA. The myocardial fibrosis and collagen volume fraction(CVF) was detected by Masson staining. The protein expression levels of Col-I and Col-Ⅲ were detected by immunohistochemical staining. The protein expressions of TGF-β1, Smad2 and p-Smad2 were determined by western blotting. Results: Compared with the sham-operation group, the LVEDP, CVF, and the levels of troponin T, CK-MB, and NT-proBNP in serum were significantly increased in the model group, while the LVSP, +dp/dtmaxand-dp/dtmaxwere significantly de-creased(P<0.05). Compared with the model group,the LVEDP, CVF, the troponin T, CK-MB and NTpro BNP levels in serum and the protein expressions ofCol-Ⅰ, Col-Ⅲ, TGF-β1 and p-Smad2 were significantly decreased in salvianolic acid A group, while the LVSP, +dp/dtmaxand-dp/dtmaxwere significantly increased(P<0.05). Conclusion: Salvianolic acid A can attenuate myocardial fibrosis and improve cardiac function in myocardial infarction rats, and the mechanism may be related to the inhibition of TGF-β1/Smad2 signaling pathway.更多还原