miRNA-33a对马拉松跑导致心肌纤维化的调控作用  

Regulatory Effect of miRNA-33a on Myocardial Fibrosis Resulted from Marathon

作　　者：徐承建[1] 祝捷[1] XU Chengjian;ZHU Jie(Guangdong Vocational Institute of Sport,Guangzhou,Guangdong 510663,China.)

机构地区：[1]广东体育职业技术学院,广东广州510663

出　　处：《首都体育学院学报》2020年第5期476-480,共5页Journal of Capital University of Physical Education and Sports

摘　　要：目的:通过动物实验建模和细胞学实验验证miRNA-33a对马拉松跑导致心肌纤维化的调控作用。方法:通过动物实验建模对实验大鼠进行马拉松跑训练,检测miRNA-33a的变化情况及心肌形态学差异,以分析实验大鼠左心室心肌纤维化对心功能的影响程度。通过细胞学实验证明miRNA-33a对CFb合成胶原蛋白、分化等的调控作用。结果:(1)检测各组大鼠的心功能状况:相比对照组(CG),实验组(EG)大鼠的左心室射血分数(LVEF)和左心室短轴缩短率(LVFS)均显著下降(P<0.05);而相比实验组(EG),miRNA-33a+EG组大鼠的LVEF显著提高、LVFS显著增长。(2)Q-PCR检测显示:与对照组(CG)相比,实验组(EG)的miRNA-33a显著上调(P<0.05);与实验组(EG)相比,miRNA-33a+EG组的miRNA-33a则显著下降(P<0.05)。(3)HE染色结果显示:miRNA-33a+EG的大鼠心肌纤维结构紊乱得到缓解,且肌细胞体积明显缩小。Masson染色结果显示:miRNA-33a+EG的大鼠胶原纤维数量显著减少,心肌纤维结构排列相对有序。与实验组(EG)相比,miRNA-33a+EG胶原蛋白容积分数显著下降(P<0.05)。(4)Western blot检测结果显示:转染miRNA-33a模拟物后,CFb细胞I型胶原蛋白、III型胶原蛋白、CTGF的蛋白含量均显著增加(P<0.05);转染miRNA-33a抑制剂后,CFb细胞I型胶原蛋白、III型胶原蛋白、CTGF的蛋白含量均显著减少(P<0.05)。(5)Western blot检测结果显示:miRNA-33a模拟物显著增加CFb细胞a-SMA的蛋白含量(P<0.05);miRNA-33a抑制剂显著降低CFb细胞a-SMA的蛋白含量(P<0.05)。结论:miRNA-33a可显著改善马拉松跑导致心肌纤维化的病理变化,为后续研究提供了干预靶点。Objective: To verify the regulation of miRNA-33a on myocardial fibrosis resulted from marathon through animal and cytological experiments. Methods: The variation of miRNA-33a in the left ventricle and the morphology of myocardial morphology is to be verified by zoological experiments, so as to analyze the degree of left ventricular fibrosis in rats. Through cytological experiments, it is to prove that miRNA-33a regulates the function of CFb synthesis of collagen and differentiation in the cytological layer. Results: 1) Determination of cardiac function in each group: Compared with control group(CG), the left ventricular ejection fraction(LVEF)and left ventricular short axis shortening rate(LVFS) of EG group were significantly lower(P<0.05) in the experimental group(EG);LVEF and LVFS in the miRNA-33a antago-miR+EG group were significantly increased in EG. 2) Q-PCR showed that the expression of miRNA-33a was significantly up-regulated in EG compared with CG(P<0.05). Compared with EG, miRNA-33a antago the expression of miRNA-33a in the-miR+EG decreased significantly(P<0.05). 3) HE staining showed that the disorder of tissue structure arrangement in miRNA-33a antago-miR+EG was alleviated, and the myocyte volume was significantly reduced. Masson staining showed that the number of collagen fibers in miRNA-33a antago-miR+EG was significantly decreased. The muscle fibers are arranged in a relatively orderly manner. Compared with EG, the collagen volume integral of the miRNA-33a antago-miR+EG significantly decreased(P<0.05). 4) Western blot analysis showed that transfection of miRNA-33a mimics increased the expression/content of type Ⅰ, type Ⅲ collagen and CTGF in CFb cells at m RNA/protein level(P<0.05);transfection of miRNA-33a inhibitor The expression/content of type Ⅰ, type Ⅲ collagen and CTGF decreased at the m RNA/protein level(P<0.05). 5.Western blot analysis showed that miRNA-33a mimics significantly increased a-SMA protein content in CFb cells(P<0.05). Transfection of miRNA-33a inhibitor significantly dec

关 键 词：miRNA-33a 马拉松 心肌纤维化 心脏成纤维细胞 

分 类 号：G804.5[文化科学—运动人体科学]