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陈志松,喻卓,曾永利.瑞舒伐他汀对急性心肌梗死大鼠心肌基质金属蛋白及炎症因子的影响[J].中国比较医学杂志,2019,29(2):66~71.
瑞舒伐他汀对急性心肌梗死大鼠心肌基质金属蛋白及炎症因子的影响
Effects of rosuvastatin on myocardial matrix metalloproteinases and inflammatory factors in rats with acute myocardial infarction
投稿时间:2018-07-30  
DOI:10.3969/j. issn. 1671 -7856. 2019. 02. 011
中文关键词:  瑞舒伐他汀  急性心肌梗死  大鼠  基质金属蛋白  炎性因子
英文关键词:rosuvastatin  acute myocardial infarction  rat  matrix metalloproteinase  inflammatory factor
基金项目:
作者单位E-mail
陈志松 昆明医科大学第一附属医院心血管内科二病区,昆明 650032 hxinyue6688@ 163.com 
喻卓 昆明医科大学第一附属医院心血管内科二病区,昆明 650032  
曾永利 昆明医科大学第一附属医院心血管内科二病区,昆明 650032 logoshes@ sina.com 
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中文摘要:
      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?
英文摘要:
      Objective To observe the changes of matrix metalloproteinases (MMPs), TIMP2, and inflammatory factors TNF-α and IL-1β in 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 10mg/ (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-1β in 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-1β proteins 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-1β in 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.
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