Effect of Guanxin V in animal model of acute myocardial infarction.
Effect of Guanxin V in animal model of acute myocardial infarction.
复制标题
冠心V号对急性心肌梗死动物模型的影响
DOI：
10.1186/s12906-021-03211-7
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发表时间：
2021-02-22
影响因子：
3.9
通讯作者：
Gu N
中科院分区：
文献类型：
--
作者：
Zhang X;Shao C;Cheng S;Zhu Y;Liang B;Gu N
急性心肌梗死（AMI）是世界范围内冠心病最严重和最致命的表现，具有极高的致残率和死亡率。我们前期研究表明冠心V （GXV）能显著改善AMI大鼠心功能和血流动力学，降低血清炎症因子水平，从而引发AMI后心室重构（VR）。方法采用左冠状动脉前降支结扎法建立叙利亚仓鼠急性心肌梗死模型。将叙利亚仓鼠随机分为4组，分别为假手术组（n= 12）、AMI组（n= 12）、GXV组（GXV 6 g/Kg/d,n= 12）和曲尼拉斯特组（Tra 105 mg/Kg/d,n= 12）。药物干预连续8周。分别于第4周和第8周测定相关生物学指标。结果与AMI组比较，GXV组和Tra组叙利亚仓鼠心肌功能得到改善，梗死面积和心脏重量指数受到限制。此外，GXV能够降低AMI叙利亚仓鼠肥大细胞数量和切酶水平。GXV显著灭活肾素-血管紧张-醛固酮系统，减轻心肌纤维化和心肌细胞凋亡，从而减缓ami后VR。结论xv通过降低心肌梗死后的酶水平和肥大细胞数量，使肾血管紧张-醛固酮系统失活，减缓心肌梗死后的VR过程。
BackgroundAcute myocardial infarction (AMI) is the most serious and lethal manifestation of coronary heart disease worldwide, presenting extremely high disability and mortality. Our previous studies have shown that Guanxin V (GXV) could significantly improve the cardiac function and the blood flow dynamics, and reduce serum levels of inflammatory factors in AMI rats, thus triggering ventricular remodeling (VR) at post-AMI.MethodsAn in vivo AMI model was established in Syrian hamsters by performing the ligation of the left anterior descending coronary artery. Syrian hamsters were randomly divided into four groups, namely Sham operation group (n= 12), AMI group (n= 12), GXV group (GXV 6 g/Kg/d,n= 12), and Tranilast group (Tra 105 mg/Kg/d,n= 12). Drug intervention was conducted for consecutive 8 weeks. Relative biological indicators were measured in the 4th and 8th week, respectively.ResultsCardiac functions were improved, and the infarcted size and heart weight index were limited in Syrian hamsters of GXV and Tra groups compared with those in AMI group. Furthermore, GXV was able to decrease the number of mast cells and chymase level in Syrian hamsters with AMI. Administration of GXV remarkably inactivated the renin-angiotension-aldosterone system, and alleviated myocardial fibrosis and cardiomyocyte apoptosis, thus slowing down VR at post-AMI.ConclusionGXV slows down the process of VR at post-AMI by reducing chymase level and mast cells number, as well as inactivating the reninangiotension-aldosterone system..
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