摘要
目的观察瑞舒伐他汀治疗急性心肌梗死(AMI)大鼠心肌组织中基质金属蛋白酶MMPs、TIMP2和炎性因子TNF-α、IL-1β的变化。方法选取健康SD大鼠通过结扎冠状动脉左前降支建立AMI模型。分为4组,对照组(仅穿线并不在冠状动脉处结扎,n=10);急性心肌梗死组(n=14);瑞舒伐他汀组(n=13):AMI建模后采用瑞舒伐他汀(10 mg/(kg·d))治疗;氯沙坦组(n=11):AMI建模后采用氯沙坦钾治疗(5 mg/(kg·d))。分别采用免疫组化法、RT-qPCR检测大鼠AMI建模后心肌组织基质金属蛋白酶mmp2、mmp9及抑制物TIMP2的表达水平,采用Western blot检测心肌组织中mmp2、mmp9及炎性因子TNF-α、IL-1β蛋白变化。结果免疫组化和RT-qPCR检测结果显示:与AMI组相比,瑞舒伐他汀组及氯沙坦组大鼠心肌mmp2、mmp9蛋白及mRNA表达水平均降低(P<0. 05); Western blot检测结果:与对照组相比,AMI组大鼠mmp9、mmp2、TNF-α、IL-1β蛋白表达水均明显升高(P<0. 05);而与AMI组相比,瑞舒伐他汀组、氯沙坦组大鼠心肌中mmp2、mmp9、TNF-α、IL-1β蛋白表达水平均下降(P<0. 05)。结论大鼠AMI建模后心肌发生纤维化因子mmp2、mmp9及炎性因子TNF-α、IL-1β升高,而瑞舒伐他汀可通过抑制心肌纤维化,降低炎性因子表达,在一定程度上对心功能起到改善作用。
Objective To observe the changes of matrix metalloproteinases(MMPs),TIMP2,and inflammatory factors TNF-αand IL-1βin the myocardium of rats with acute myocardial infarction(AMI)treated with rosuvastatin.Methods Healthy SD rats were selected to establish an AMI model by ligation of the left anterior descending coronary artery.They were divided into four groups:a control group(isolation of anterior descending branch without ligation,n=10);an acute myocardial infarction group(AMI modeling group);a rosuvastatin group(n=13,AMI treated with rosuvastatin at 10 mg/(kg·d)after modeling);and a losartan group(n=11,AMI treated with losartan potassium at 5 mg/(kg·d)after modeling).Immunohistochemical staining and RT-qPCR were used to determine the expression levels of MMP2,MMP9,and inhibitor TIMP2 in rat cardiac tissues after AMI modeling.Western blotting was used to determine the changes of MMP2,MMP9,TNF-α,and IL-1βin myocardium.Results The results of immunohistochemical and RT-qPCR analyses showed that,compared with those in the AMI group,the MMP2 and MMP9 protein/mRNA expression levels in rat myocardium in the rosuvastatin and losartan groups were decreased(P<0.05).Regarding the western blotting results,compared with that in the control group,the expressions of MMP9,MMP2,TNF-α,and IL-1βproteins in the AMI group were significantly increased(P<0.05).Moreover,compared with those in the AMI group,the expression levels of MMP2,MMP9,TNF-α,and IL-1βin the myocardium of the rosuvastatin and losartan groups were decreased(P<0.05).Conclusions Myocardial fibrosis factors and inflammatory factors are increased after AMI modeling in rats.Rosuvastatin can improve the cardiac function to some extent by inhibiting myocardial fibrosis and reducing the expression of inflammatory factors.
作者
陈志松
喻卓
曾永利
CHEN Zhisong;YU Zhuo;ZENG Yongli(Department of Cardiology,the First Affiliated Hospital of Kunming Medical University,Kunming 650032,China)
出处
《中国比较医学杂志》
CAS
北大核心
2019年第2期66-71,共6页
Chinese Journal of Comparative Medicine
基金
云南省科技计划项目(2015FB037)
关键词
瑞舒伐他汀
急性心肌梗死
大鼠
基质金属蛋白
炎性因子
rosuvastatin
acute myocardial infarction
rat
matrix metalloproteinase
inflammatory factor
