Background

Yiqi-Huoxue granule (YQHX), consisting of four kinds of traditional Chinese medicine, is an empirical prescription for the treatment of coronary heart disease. It is known to promote angiogenesis, but the mechanism is unknown.

Purpose

This article investigates the possible mechanism of YQHX inducing angiogenesis in the ischemic myocardium.

Methods

EAhy.926 cells were treated with YQHX hypoxic cardiomyocyte-conditioned medium (YHMCM) and the levels of VEGF, CD34, and phosphorylation of PI3K/Akt were detected by western blotting. Also, the effects on endothelial tube formation and migration were observed. The level of miR-126 was detected by qRT-PCR.

Results

YQHX promoted tube formation and migration of EAhy.926 cells and upregulated VEGF, CD34, and the phosphorylation of PI3K/AKT via regulating miR-126 levels. However, these effects were inhibited by a miR-126 inhibitor.

Conclusion

In summary, YQHX improves angiogenesis by regulating the miR-126/PI3K/Akt signaling pathway, which indicates that YQHX could be a promising therapeutic strategy for ischemic myocardium.

中文翻译：

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益气活血颗粒通过内皮细胞miR-126/PI3K/Akt轴促进缺血心肌血管生成

背景

益气活血颗粒（YQHX）由四种中药组成，是治疗冠心病的经验方。已知可促进血管生成，但其机制尚不清楚。

目的

本文探讨了益气活血诱导缺血心肌血管生成的可能机制。

方法

EAhy.926细胞用YQHX缺氧心肌细胞条件培养基（YHMCM）处理，并通过蛋白质印迹检测VEGF、CD34和PI3K/Akt的磷酸化水平。此外，观察到对内皮管形成和迁移的影响。通过qRT-PCR检测miR-126的水平。

结果

YQHX 通过调节 miR-126 水平促进 EAhy.926 细胞的管形成和迁移，并上调 VEGF、CD34 和 PI3K/AKT 的磷酸化。然而，这些作用被 miR-126 抑制剂抑制。

结论

总之，YQHX 通过调节 miR-126/PI3K/Akt 信号通路改善血管生成，这表明 YQHX 可能是一种有前途的缺血性心肌治疗策略。