基质金属蛋白酶3对大鼠心肌纤维化细胞活力的影响  

Effects of Matrix Metalloproteinase 3 on the Viability of Myocardial Fibrosis Cells in Rats

作　　者：舒锦 汪海娅[2] 金立 Shu Jin;Wang Haiya;Jin Li(Department of Gerontology,Shibei Hospital of Jing'an District,Shanghai,200443,P.R.China;Department of Gerontology,Renji Hospital Affiliated to School of Medicine of Shanghai Jiaotong University,Shanghai,200001,P.R.ChinaChina)

机构地区：[1]上海市静安区市北医院老年科,上海200443 [2]上海交通大学医学院附属仁济医院老年科,上海200001

出　　处：《老年医学与保健》2020年第3期476-479,492,共5页Geriatrics & Health Care

基　　金：上海市静安区科学技术委员会(面上2020MS12)。

摘　　要：目的探讨基质金属蛋白酶3(MMP3)对心肌纤维化细胞活力的影响。方法利用MMP3过表达载体及siRNA-MMP3转染大鼠心肌细胞H9C2,并用荧光定量PCR(RT-qPCR)检测转染效率。用不同浓度的血管紧张素II(AngII)处理H9C2细胞不同时间,通过RT-qPCR检测细胞中Axl基因的表达情况。最后用CCK-8试剂盒检测MMP3过表达和敲低对心肌纤维化细胞活力的影响。结果RT-qPCR结果表明MMP3过表达和敲低的H9C2细胞成功构建,并且10-8 M AngII处理H9C2细胞24 h后,Axl的mRNA表达水平与未处理的相比降低(P<0.01)。CCK-8检测结果表明,与正常心肌细胞相比,心肌纤维化细胞的活力下降(P<0.05)。当心肌纤维化细胞中MMP3敲低后,其细胞活性进一步降低(P<0.05);当用100 M左卡尼汀处理后,其活力的变化趋势与敲低后的相似。而当MMP3过表达时,其细胞活性与用左卡尼汀处理正常细胞的相比增加(P<0.05)。结论MMP3敲低可能通过降低心肌纤维化细胞的活力,抑制细胞增殖,从而可能改善心肌纤维化,延缓心肌重构。Objective To investigate the effects of matrix metallopeptidase 3(MMP3)on the viability of myocardial fibrosis cells.Methods Rat cardiomyocyte H9 C2 were transfected with MMP3 overexpression vector and siRNA-MMP3,and the transfection efficiency was determined by fluorescence quantitative PCR(RT-qPCR).The different concentrations of Ang II were used to treat H9 C2 cells for different times,and then the expression of Axl was detected by RT-qPCR.Finally,the effects of MMP3 overexpression and knockdown on the viability of myocardial fibrotic cells was tested with CCK-8 kit.Results RT-qPCR showed that H9 C2 cells with overexpression and knockdown of MMP3 were successfully constructed,and the m RNA expression level of Axl in H9 C2 cells treated with 10-8 M Ang II was significantly lower than that in untreated cells(P<0.05).CCK-8 test results showed that compared with normal cardiomyocytes,the viability of myocardial fibrotic cells decreased(P<0.05).When MMP3 was knocked down in myocardial fibrotic cells,its cell viability was further reduced(P<0.05);when treated with 100 M levocarnitine,the change trend of its vitality was similar to that after knocking down;when MMP3 was overexpressed,its cell viability increased compared with that of normal cells treated with L-carnitine(P<0.05).Conclusion MMP3 knockdown may improve myocardial fibrosis and delay myocardial remodeling by reducing the activity of myocardial fibrosis cells and inhibiting cell proliferation.

关 键 词：心肌细胞纤维化 基质金属蛋白酶3(MMP3) 血管紧张素Ⅱ(AngⅡ) 细胞活力 

分 类 号：R965[医药卫生—药理学]