电针通过调节内源性干细胞的动员和迁移来改善心肌梗死后的心功能。

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS
ACS Applied Bio Materials Pub Date : 2023-12-01 Epub Date: 2023-06-19 DOI:10.1177/09645284231169485
Shou-Song Xuan, Yue Zhao, Yan Zheng, Jing Zhu, Han Li, Ping-Ping Lu, Shui-Jin Shao, Hai-Dong Guo, Fang-Fang Mou
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引用次数: 0

摘要

目的:探讨电针(EA)在心肌梗死(MI)后内源性干细胞动员和心肌再生过程中趋化因子调控中的作用及机制。方法:结扎左冠状动脉前降支,建立成年雄性sd大鼠心肌梗死模型。治疗4周后,超声心动图检测心功能变化,马松三色染色检测胶原沉积。此外,采用免疫荧光染色法检测梗死区血管性血变因子(vWF)阳性血管、心肌肌钙蛋白T (cTnT)和增殖标志物Ki67的表达以及c-kit阳性、C-X-C趋化因子受体4型(CXCR4)阳性和sca -1阳性内源性干细胞的数量。此外,检测基质细胞衍生因子(SDF)-1和干细胞因子(SCF)的表达。结果:与未治疗模型组比较,EA可提高心肌梗死后的射血分数,减少胶原沉积和细胞凋亡,增加血管数量。EA显著促进了除心肌细胞外的细胞增殖,显著增加了c-kit-、CXCR4-和sca -1阳性干细胞的数量。此外,EA组心肌组织中SDF-1和SCF的表达明显高于(未治疗)MI组。结论:EA可促进心肌梗死大鼠血管生成,减少胶原沉积,从而改善心肌功能,其作用机制可能与SDF-1/CXCR4和SCF/c-kit介导的内源性干细胞动员有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Electroacupuncture improves cardiac function after myocardial infarction by regulating the mobilization and migration of endogenous stem cells.

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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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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