YQHX Alleviates H/R-Induced Cardiomyocyte Apoptosis by Downregulating miR-1.
Luandie GeYaqi FanLin FuMengjiao GuoPanxia CaoChaojie PengLinke WuLihua HanHong WuPublished in: Evidence-based complementary and alternative medicine : eCAM (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 (p < 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 (p < 0.01 or p < 0.05). We also found that miR-1 overexpression could enhance apoptosis in cardiomyocytes, whereas apoptosis could be reduced by YQHX treatment (p < 0.01). In conclusion, YQHX alleviates H/R-induced cardiomyocyte apoptosis by inhibiting miR-1 expression, suggesting the potential of YQHX in preventing MIRI.
Keyphrases
- cell cycle arrest
- induced apoptosis
- endoplasmic reticulum stress
- cell death
- oxidative stress
- pi k akt
- cell proliferation
- high glucose
- long non coding rna
- ischemia reperfusion injury
- diabetic rats
- signaling pathway
- poor prognosis
- long noncoding rna
- left ventricular
- endothelial cells
- heart failure
- angiotensin ii
- binding protein
- protein kinase
- drug induced
- atrial fibrillation
- human health
- stress induced
- smoking cessation