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电可以通过调节内源干细胞的动员和迁移来改善心肌梗塞后的心脏功能
Shou-Song Xuan1,2, Yue Zhao1,3, Yan Zheng2
1Department of Anatomy, School of Basic Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
概括
电针 (EA) 通过促进干细胞动员和血管生成,增强心肌梗塞 (MI) 后的心脏功能. 这种治疗可能涉及树皮细胞衍生因子-1 (SDF-1) /CXCR4和干细胞因子 (SCF) /c-kit通路.
科学领域:
- 心血管研究研究心血管研究
- 再生医学是一种再生医学.
- 干细胞生物学 干细胞生物学
背景情况:
- 心肌梗塞 (MI) 导致严重的心脏功能障碍和有限的内源性修复机制.
- 化学基因在干细胞招募和MI后组织再生中发挥着至关重要的作用.
- 电针 (EA) 是心血管疾病的潜在治疗方式.
研究的目的:
- 调查电针 (EA) 在调节内源干细胞调动和心肌梗塞 (MI) 后心肌再生的化学因子中的作用.
- 阐明EA对心脏功能后心脏病发作的治疗作用的潜在机制.
主要方法:
- 通过绑定左前垂下垂冠状动脉,建立了一个MI老鼠模型.
- 心声扫描评估了心脏功能; 马森三色染色评估了原沉积.
- 免疫光检测到血管化 (vWF),增殖 (Ki67),亡,以及干细胞标记物 (c-kit,CXCR4,Sca-1),以及化学激素表达 (SDF-1,SCF).
主要成果:
- 与对照组相比,EA治疗改善了射出分数,减少了原沉积和亡,增加了血管化.
- EA显著促进细胞增殖,并增加了c-kit,CXCR4和Sca-1阳性干细胞的数量.
- 在EA治疗后,肌肉细胞衍生因子-1 (SDF-1) 和干细胞因子 (SCF) 的表达在心肌组织中显著增加.
结论:
- 电针有效地促进血管生成,减少原沉积,从而改善心脏功能在MI的老鼠模型.
- EA的治疗机制可能涉及通过SDF-1/CXCR4和SCF/c-kit信号通路调动内源干细胞.
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