Electroacupuncture improves cardiac function after myocardial infarction by regulating the mobilization and migration of endogenous stem cells

医学 基质细胞衍生因子1 干细胞 内科学 肌钙蛋白复合物 心脏标志物 马森三色染色 心功能曲线 肌钙蛋白T 心肌梗塞 内生 干细胞疗法 干细胞因子 血管生成 射血分数 内分泌学 CXCR4型 趋化因子 祖细胞 受体 肌钙蛋白I 细胞生物学 心力衰竭 肌钙蛋白 生物 纤维化 移植
作者
Shou-Song Xuan,Yue Zhao,Yan Zheng,Jing Zhu,Li Han,Pingping Lu,Shui-jin Shao,Hai-dong Guo,Fang-fang Mou
出处
期刊:Acupuncture in Medicine [SAGE Publishing]
卷期号:41 (6): 354-363
标识
DOI:10.1177/09645284231169485
摘要

Objective: The aim of this study was to explore the role and mechanisms of electroacupuncture (EA) in the regulation of chemokines in endogenous stem cell mobilization and myocardial regeneration after myocardial infarction (MI). Methods: An MI model was constructed in adult male Sprague-Dawley rats by ligating the left anterior descending coronary artery. After 4 weeks of treatment, echocardiography was used to detect changes in cardiac function, and Masson’s trichrome staining was used to detect collagen deposition. In addition, immunofluorescence staining was applied to examine von Willebrand factor (vWF)-positive vessels, the expression of cardiac troponin T (cTnT) and proliferation marker Ki67, and the number of c-kit-positive, C-X-C chemokine receptor type 4 (CXCR4)-positive, and Sca-1-positive endogenous stem cells in the infarcted area. In addition, the expression of stromal cell-derived factor (SDF)-1 and stem cell factor (SCF) was detected. Results: EA increased the ejection fraction after MI, reduced collagen deposition and cellular apoptosis, and increased the number of blood vessels compared with an untreated model group. EA significantly promoted cellular proliferation, except for myocardial cells, and significantly increased the number of c-kit-, CXCR4- and Sca-1-positive stem cells. Moreover, the expression of SDF-1 and SCF in myocardial tissue in the EA group was significantly higher than that in the (untreated) MI group. Conclusions: EA appears to promote angiogenesis and reduce collagen deposition, thus improving the cardiac function of rats with MI. The underlying mechanism of action may involve endogenous stem cell mobilization mediated by SDF-1/CXCR4 and SCF/c-kit.
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