阿佩林-13通过调节巨细胞两极分化来改善心肌缺血/反损伤
Hui Jia1, Qiyue Zhao1, Jing Yuan2
1Department of Physiology, Hebei Medical University, Shijiazhuang Medical College, Shijiazhuang, 050017, Hebei, China.
Archives of biochemistry and biophysics
|December 22, 2025
概括
阿佩林-13通过将巨转移到修复性M2表型并减少心脏细胞亡,改善心肌缺血/反 (I/R) 损伤后的心脏功能. 这种在治疗I/R损伤方面表现有前途.
科学领域:
- 心脏病学 心脏病学
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 巨细胞两极分化极大地影响心肌缺血/反 (I/R) 损伤的结果.
- 在心肌I/R损伤期间调节巨细胞两极分化的Apelin-13的治疗潜力尚不清楚.
研究的目的:
- 在大鼠心肌I/R模型中研究阿佩林-13对巨分极和心脏功能的影响.
- 在体外探索Apelin-13对H9c2细胞的影响.
主要方法:
- 在老鼠中诱导的心肌I / R损伤;H9c2细胞和老鼠腹膜巨细胞在体外培养.
- 评估心脏功能,心脏病发作大小,细胞亡和巨细胞极化标志物 (M1/M2).
- 评估了阿佩林-13对细胞因子产生和H9c2细胞存活在氧气-葡萄糖剥夺/再氧化条件下的影响.
主要成果:
- 在老鼠I/R模型中,阿佩林-13显著改善了心脏功能,并减少了心脏病发作的大小.
- 阿佩林-13治疗降低了心肌亡,并在体内促进了从M1转向M2巨细胞两极分化的转变.
- 在体外,Apelin-13抑制了促炎性细胞因子,增强了M2标记物,并改善了H9c2细胞存活率.
结论:
- 阿佩林-13在肌肉心脏I/R损伤方面显示出治疗潜力.
- 调节巨细胞极化和减少心肌细胞亡是阿佩林-13保护作用的关键机制.
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