摘要
目的观察大鼠心肌梗死后转化生长因子-β1(TGF-β1)、p38丝裂原活化蛋白激酶(p38MAPK)以及p-p38MAPK的动态变化,探讨它们在心室重塑过程中的作用。方法结扎雄性SD大鼠冠状动脉前降支建立心肌梗死模型,并设假手术组为对照。术后1、7、14和21d检测大鼠血流动力学指标,HE染色观察梗死区域组织病理变化;Westernblot检测心肌组织TGF-β1、p38MAPK以及p-p38MAPK蛋白的表达水平。结果与假手术组相比,心肌梗死组大鼠心脏功能明显下降,心肌梗死大鼠心肌纤维化程度逐渐增加,心肌组织TGF-β1蛋白表达进行性增加,p38MAPK蛋白表达基本不变,而磷酸化蛋白p-p38MAPK表达则是先上升后下降。结论大鼠心肌梗死后TGF-β1蛋白表达逐渐升高,它的升高可能激活了p38MAPK的磷酸化过程,TGF-β1是大鼠心肌梗死后心室重塑病理生理过程中的重要因子之一。
Objective To analyze the dynamic changes of transforming growth factor（TGF）-β1 and p38 mitogen-activated protein kinase（p38MAPK） and p-p38MAPK in the ventricular remodeling process of rat after myocardial infarction （MI） and reveal the roles of them in this process. Methods Rat models of MI were established by ligation of the left coronary （group MI） and sham operated rats were taken as the controls （group C）. Hemodynamic changes were recorded on the 1st , 7th, 14th , 21st day after operation. The infarcted areas were observed by hematoxylin-eosin staining. The protein levels of TGF-β1 ,p38MAPK and the p-p38MAPK were determined by Western blot analysis. Results The hemodynamic differences were remarkable between group MI and group C. The fibrosis of cardiac tissue was gradually progressed. The protein levels of TGF-β1 were increased step by step and the expressions of p38MAPK protein remained unchanged after MI, but the expression of p-p38MAPK in group MI reached their peaks on the 7th day after MI and reduced afterwards. Conclusion TGF-β1 was increased gradually after MI, which may activate the phosphorylation of p38MAPK and be one of the most possible mechanisms in the ventricular remodeling of MI rats.
出处
《江苏医药》
CAS
CSCD
北大核心
2009年第3期329-331,共3页
Jiangsu Medical Journal
关键词
心肌梗死
心室重塑
转化生长因子-Β1
P38丝裂原活化蛋白激酶
Myocardial infarctiom Ventricular remodeling
Transforming growth factor TGF-β1 （TGF-β1）
p38 Mitogen-activated protein kinase（p38MAPK）
