益气活血方通过下调miR-1减轻缺氧/复氧诱导的心肌细胞凋亡。

YQHX Alleviates H/R-Induced Cardiomyocyte Apoptosis by Downregulating miR-1.

作者信息

Ge Luandie, Fan Yaqi, Fu Lin, Guo Mengjiao, Cao Panxia, Peng Chaojie, Wu Linke, Han Lihua, Wu Hong

机构信息

Graduate School, Henan University of Chinese Medicine, Zhengzhou 450046, China.

Institute of Cardiovascular Disease, Henan University of Chinese Medicine, Zhengzhou 450002, China.

出版信息

Evid Based Complement Alternat Med. 2021 Nov 2;2021:4852406. doi: 10.1155/2021/4852406. eCollection 2021.

Yiqi Huoxue granule (YQHX) inhibits cardiomyocyte apoptosis in myocardial ischemia-reperfusion injury (MIRI); however, the underlying mechanism is unknown. In this study, hypoxia-reoxygenation (H/R) models were established using rat myocardial primary cells and H9c2 cells, lactate dehydrogenase (LDH), and creatine kinase (CK) levels and cardiomyocyte apoptosis were determined. LDH release, CK activity, caspase-3 activation, mRNA and protein ratio of Bax/Bcl-2, and miR-1 expression were significantly higher ( < 0.01) in the H/R model of rat myocardial primary cells and H9c2 cells compared with the control group and was inhibited by YQHX treatment ( < 0.01 or < 0.05). We also found that miR-1 overexpression could enhance apoptosis in cardiomyocytes, whereas apoptosis could be reduced by YQHX treatment ( < 0.01). In conclusion, YQHX alleviates H/R-induced cardiomyocyte apoptosis by inhibiting miR-1 expression, suggesting the potential of YQHX in preventing MIRI.

益气活血颗粒（YQHX）可抑制心肌缺血再灌注损伤（MIRI）中的心肌细胞凋亡；然而，其潜在机制尚不清楚。在本研究中，使用大鼠心肌原代细胞和H9c2细胞建立缺氧复氧（H/R）模型，测定乳酸脱氢酶（LDH）、肌酸激酶（CK）水平及心肌细胞凋亡情况。与对照组相比，大鼠心肌原代细胞和H9c2细胞的H/R模型中LDH释放、CK活性、caspase-3激活、Bax/Bcl-2的mRNA和蛋白比值以及miR-1表达均显著升高（<0.01），而YQHX处理可抑制上述指标（<0.01或<0.05）。我们还发现，miR-1过表达可增强心肌细胞凋亡，而YQHX处理可减少凋亡（<0.01）。综上所述，YQHX通过抑制miR-1表达减轻H/R诱导的心肌细胞凋亡，提示YQHX在预防MIRI方面具有潜在应用价值。