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用于心肌梗死后重塑的非马沙坦

Fimasartan for Remodeling after Myocardial Infarction.

作者信息

Lim Byung-Kwan, Park Jin Joo, Park Sung-Ji, Lee You-Jung, Kwon Jin-Sook, Kim Eun-Ji, Choi Dong-Ju

机构信息

Department of Biomedical Science, Jungwon University, Goesan-gun 28024, Korea.

Department of Internal Medicine, College of Medicine, Seoul National University Bundang Hospital, Seongnam 13620, Korea.

出版信息

J Clin Med. 2019 Mar 15;8(3):366. doi: 10.3390/jcm8030366.

Abstract

An angiotensin receptor blocker (ARB) mitigates cardiac remodeling after myocardial infarction (MI). Here, we investigated the effect of fimasartan, a new ARB, on cardiac remodeling after MI. Sprague⁻Dawley rats were assigned into 3 groups: surgery only (sham group, = 7), MI without (MI-only group, = 13), and MI with fimasartan treatment (MI + Fima group, = 16). MI was induced by the permanent ligation of the left anterior descending artery. Treatment with fimasartan (10 mg/kg) was initiated 24 h after MI and continued for 7 weeks. Rats in the MI + Fima group had a higher mean ejection fraction (66.3 ± 12.5% vs. 51.3 ± 14.8%, = 0.002) and lower left ventricular end-diastolic diameter (9.14 ± 1.11 mm vs. 9.91 ± 1.43 mm, = 0.045) than those in the MI-only group at 7 weeks after MI. The infarct size was lower in the MI + Fima than in the MI group ( < 0.05). A microarray analysis revealed that the expression of genes related to the lipid metabolism and mitochondrial membrane ion transporters were upregulated, and those involved in fibrosis and inflammation were downregulated by fimasartan. Fimasartan attenuates cardiac remodeling and dysfunction in rats after MI and may prevent the progression to heart failure after MI.

摘要

血管紧张素受体阻滞剂(ARB)可减轻心肌梗死后的心脏重塑。在此,我们研究了新型ARB药物非马沙坦对心肌梗死后心脏重塑的影响。将Sprague-Dawley大鼠分为3组:仅手术组(假手术组,n = 7)、未治疗的心肌梗死组(单纯心肌梗死组,n = 13)和接受非马沙坦治疗的心肌梗死组(心肌梗死+非马沙坦组,n = 16)。通过永久性结扎左冠状动脉前降支诱导心肌梗死。心肌梗死后24小时开始用非马沙坦(10 mg/kg)治疗,并持续7周。心肌梗死+非马沙坦组大鼠在心肌梗死后7周时的平均射血分数高于单纯心肌梗死组(66.3±12.5%对51.3±14.8%,P = 0.002),左心室舒张末期直径低于单纯心肌梗死组(9.14±1.11 mm对9.91±1.43 mm,P = 0.045)。心肌梗死+非马沙坦组的梗死面积低于心肌梗死组(P < 0.05)。基因芯片分析显示,非马沙坦上调了与脂质代谢和线粒体膜离子转运体相关的基因表达,下调了与纤维化和炎症相关的基因表达。非马沙坦可减轻大鼠心肌梗死后的心脏重塑和功能障碍,并可能预防心肌梗死后进展为心力衰竭。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da2/6463200/08e0f7a5c956/jcm-08-00366-g001.jpg

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