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丹芪软胶囊通过减轻线粒体分裂来减轻心肌缺血再灌注损伤诱导的心肌细胞凋亡。

Danqi soft caspule alleviates myocardial ischemia-reperfusion injury induced cardiomyocyte apoptosis by attenuating mitochondrial fission.

作者信息

Yang Ye, Lin Cuiting, Wang Yan, Liu Yu, Chen Qiuxiong, Ma Shiyu, Ma Jin

机构信息

The Second Clinical College of Guangzhou University of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China.

State Key Laboratory of Dampness Syndrome of Chinese Medicine, Guangzhou, China.

出版信息

Front Pharmacol. 2025 Mar 12;16:1526253. doi: 10.3389/fphar.2025.1526253. eCollection 2025.

Abstract

BACKGROUND

Myocardial ischemia-reperfusion (I/R) injury which leads to continuously worsening ventricular remodeling and cardiac dysfunction in the chronic stage, is a significant contributor to the global prevalence of heart failure. Traditional Chinese herbal formulas have been shown to prevent myocardial I/R injury.

METHOD

This study aims to investigate whether Danqi soft caspule (DQ), a classical traditional Chinese medicine (TCM) preparation, exerted the protective effects against myocardial I/R injury and explore the potential underlying mechanisms. A rat model of myocardial I/R and a cell model of HO induced oxidative stress injury were established to assess the effects of DQ on cardiac injury, cardiomyocyte apoptosis, as well as mitochondrial structure and function.

RESULT

DQ pre-treatment reduced both the proportion of infarct area and ischemic risk area and decreased cardiomyocyte apoptosis in myocardial I/R injury rats. In HO induced cells, DQ was found to reduce cell apoptosis and lower oxidative stress levels. Furthermore, DQ inhibited mitochondrial fission, prevented alterations in mitochondrial membrane potential, and suppressed Cytochrome C release from the mitochondria, thereby preventing apoptosis. DQ has protective effects against I/R induced oxidative stress injury by reducing cardiomyocyte apoptosis through inhibition mitochondrial fission. Moreover, DQ could restore mitochondrial structure and function by suppressing the phosphorylation of Ca/calmodulin-dependent protein kinase II (CaMKII) and dynamin-related protein 1 (Drp-1).

CONCLUSION

DQ inhibited I/R injury and cardiomyocyte apoptosis by reducing mitochondrial fission associated with suppressing the phosphorylation of CaMKII and Drp-1.

摘要

背景

心肌缺血再灌注(I/R)损伤在慢性期会导致心室重构和心脏功能障碍不断恶化,是全球心力衰竭患病率的一个重要促成因素。已证明中药复方制剂可预防心肌I/R损伤。

方法

本研究旨在探讨经典中药制剂丹芪软胶囊(DQ)是否对心肌I/R损伤具有保护作用,并探索其潜在的作用机制。建立心肌I/R大鼠模型和过氧化氢(HO)诱导的氧化应激损伤细胞模型,以评估DQ对心脏损伤、心肌细胞凋亡以及线粒体结构和功能的影响。

结果

DQ预处理降低了心肌I/R损伤大鼠的梗死面积比例和缺血危险面积,并减少了心肌细胞凋亡。在HO诱导的细胞中,发现DQ可减少细胞凋亡并降低氧化应激水平。此外,DQ抑制线粒体分裂,防止线粒体膜电位改变,并抑制细胞色素C从线粒体释放,从而防止细胞凋亡。DQ通过抑制线粒体分裂减少心肌细胞凋亡,对I/R诱导的氧化应激损伤具有保护作用。此外,DQ可通过抑制钙/钙调蛋白依赖性蛋白激酶II(CaMKII)和动力相关蛋白1(Drp-1)的磷酸化来恢复线粒体结构和功能。

结论

DQ通过减少与抑制CaMKII和Drp-1磷酸化相关的线粒体分裂来抑制I/R损伤和心肌细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e93/11936904/3c9b300abd33/fphar-16-1526253-g001.jpg

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