[1]刘 放,谈 红,晋 群,等.阿托伐他汀改善急性心肌梗死后左室收缩功能实验研究[J].陕西医学杂志,2022,51(10):1196-1200.[doi:DOI:10.3969/j.issn.1000-7377.2022.10.005]
　LIU Fang,TAN Hong,JIN Qun,et al.Mechanism of atorvastatin improving the left ventricular systolic function after acute myocardial infarction in rabbits[J].,2022,51(10):1196-1200.[doi:DOI:10.3969/j.issn.1000-7377.2022.10.005]
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阿托伐他汀改善急性心肌梗死后左室收缩功能实验研究
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《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
51
期数:
2022年10期
页码:
1196-1200
栏目:
基础研究
出版日期:
2022-10-05

文章信息/Info

Title:
Mechanism of atorvastatin improving the left ventricular systolic function after acute myocardial infarction in rabbits
作者:
刘 放1; 谈 红2; 晋 群2; 韩淑芳2;  陈瑞敏2; 杨 燕2
(1.锦州医科大学研究生培养基地 解放军第九六〇医院,山东 济南250031; 2.解放军第九六〇医院心内科,山东 济南250031)
Author(s):
LIU Fang; TAN Hong; JIN Qun; HAN Shufang; CHEN Ruimin; YANG Yan
(Postgraduate Training Base,the 960th Hospital of PLA,Jinzhou Medical University,Jinan 250031,China)
关键词:
急性心肌梗死;  阿托伐他汀;  血管新生;  左室收缩功能;  微小RNA126;  微小RNA221
Keywords:
Acute myocardial infarction;  Atorvastatin;  Angiogenesis;  Left ventricle systolic function;  miR-126;  miR-221
分类号:
R 542.2
DOI:
DOI:10.3969/j.issn.1000-7377.2022.10.005
文献标志码:
A
摘要:
目的:探讨不同剂量阿托伐他汀对兔急性心肌梗死后心肌组织微小RNA126(miR-126)和微小RNA221(miR-221)表达、血管新生及左室收缩功能的影响。方法:建立兔急性前壁心肌梗死模型,随机均分为对照组、急性心肌梗死(AMI)组和低剂量阿托伐他汀组、高剂量阿托伐他汀组。4周时超声心动图测定左心室射血分数(LVEF)、每搏输出量(SV)、左心室短轴缩短率(LVFS),然后取梗死区心肌组织,免疫组化法检测梗死区心肌组织微血管密度(MVD)、 RT-PCR法检测心肌miR-126和miR-221表达。结果:与对照组比较,AMI组心肌miR-126表达显著下调,miR-221表达显著上调(均P<0.01),LVEF、SV、LVFS显著降低(均P<0.01)。阿托伐他汀治疗后,心肌组织 miR-126表达水平较AMI组明显增高,miR-221水平显著降低(均P<0.01),梗死组织MVD显著增高(P<0.01),LVEF、SV、LVFS有一定程度增加(均P<0.01),以上变化在高剂量他汀组更为显著。梗死心肌组织MVD与miR-126表达呈显著正相关(r=0.703,P<0.05),与miR-221表达呈显著负相关(r=-0.755,P<0.01)。结论: 阿托伐他汀可能通过调控miR-126和miR-221的表达,促进心肌梗死后梗死心肌组织的血管新生,进而改善左室收缩功能,且作用呈剂量依赖性。
Abstract:
Objective:To investigate the effects of different doses of atorvastatin on the expression of miR-126 and miR-221,angiogenesis and left ventricular systolic function after acute myocardial infarction in rabbits.Methods:Rabbit models of acute anterior myocardial infarction were established and randomly divided into control group,acute myocardial infarction(AMI)group,low-dose atorvastatin group and high-dose atorvastatin group.Left ventricular ejection fraction(LVEF),stroke volume(SV)and left ventricular fractional shortening(LVFS)were measured by echocardiography at 4 weeks.Then myocardial tissue was taken from infarcted area,and microvessel density(MVD)was detected by immunohistochemistry,and myocardial miR-126 and miR-221 expression were detected by RT-PCR.Results:Compared with control group,the expression of miR-126 in the AMI group was significantly down-regulated,and the expression of miR-221 was significantly up-regulated,and the LVEF,SV and LVFS were significantly decreased(all P<0.01).After atorvastatin treatment,the expression level of miR-126 in myocardial tissue was significantly higher than that in the AMI group,and the level of miR-221 was significantly decreased(all P<0.01),and the MVD in infarcted tissue was significantly increased(P<0.01),and LVEF,SV,LVFS increased to a certain extent(all P<0.01),and the above changes were more significant in the high-dose statin group.MVD in infarcted myocardial tissue was significantly positively correlated with the expression of miR-126(r=0.703,P<0.05),and significantly negatively correlated with the expression of miR-221(r=-0.755,P<0.01).Conclusion:Atorvastain may promote angiogenesis in infarcted myocardial tissue by regulating the expression of miR-126 and miR-221,then improved left ventricular systolic function,and these effects were dose-dependent.

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更新日期/Last Update: 2022-10-07