S100A8/A9对心脏成纤维细胞纤维化的影响  

Effect of S100A8/A9 on cardiac fibroblasts

作　　者：何华宾[1] 罗煜 温军 郭哲 吴冰 HE Hua-bin;LUO Yu;WEN Jun;GUO Zhe;WU Bing(Gannan Medical University Dept.of Orthopaedics,the First Affiliated Hospital,Ganzhou,Jiangxi 341000;Gannan Medical University,Ganzhou,Jiangxi 341000;Gannan Medical University School of Basic Medicine,Ganzhou,Jiangxi 341000)

机构地区：[1]赣南医学院第一附属医院骨科,江西赣州341000 [2]赣南医学院,江西赣州341000 [3]赣南医学院基础医学院,江西赣州341000

出　　处：《赣南医学院学报》2019年第12期1189-1192,共4页JOURNAL OF GANNAN MEDICAL UNIVERSITY

基　　金：国家自然科学基金项目(81560039);赣南医学院校级课题(YB201310)

摘　　要：目的:观察S100A8/A9对心脏成纤维细胞纤维化的影响。方法:血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)刺激心脏成纤维细胞,建立心脏纤维化细胞模型。MTT法检测细胞增殖,Real-time PCR检测Ⅰ型和Ⅲ型胶原蛋白mRNA表达水平。结果:AngⅡ+S100A8/A9组与AngⅡ组相比较,细胞增殖受到抑制(P<0.05),Ⅰ型和Ⅲ型胶原蛋白mRNA表达水平亦下调(P<0.05)。结论:S100A8/A9可抑制AngⅡ诱导的心脏成纤维细胞增殖和纤维化标志物的表达。Objective:To observe the effect of S100 A8/A9 on cardiac fibrosis.Methods:Cardiac fibroblasts were stimulated by AngⅡto establish a cell model of cardiac fibrosis.MTT was used to detect the cell proliferation.The mRNA expression levels of CollagenⅠandⅢwas determined by Real-time PCR.Results:Compared with AngⅡgroup,the proliferation of cardiac fibrosis was depressed in AngⅡ+S100 A8/A9 group(P<0.05).The mRNA expression levels of CollagenⅠandⅢwere also down-regulated(P<0.05).Conclusions:S100 A8/A9 can inhibit the proliferation and the expression levels of cardiac fibrosis biomarkers induced by AngⅡ.

关 键 词：S100A8/A9 心脏成纤维细胞 细胞增殖 心肌纤维化 

分 类 号：R322.11[医药卫生—人体解剖和组织胚胎学]