Phlorizin allevistes oxidative stress and apoptosis of rat cardiac myocytes H9C2 induced by hypoxia/reoxygenation by down-regulating miR-125a-5p
- VernacularTitle:根皮苷通过下调miR-125a-5p减轻缺氧/复氧诱导的H9C2细胞氧化应激和凋亡
- Author:
Chunbo MIAO
1
;
Yingchun XU
;
Yifang CHANG
Author Information
- Keywords: myocardial reperfusion injury; cell hypoxia; myocardium; microRNAs; apoptosis; oxidative stress; Phlorizin; miR-125a-5p
- From: Tianjin Medical Journal 2024;52(12):1233-1238
- CountryChina
- Language:Chinese
- Abstract: Objective To investigate the effect of phlorizin on the apoptosis and oxidative stress of rat cardiomyocytes H9C2 induced by hypoxia/reoxygenation(H/R)and its possible mechanism.Methods H9C2 cells were cultured in vitro.H/R model was established after pretreatment with different doses(16,32,64 μmol/L)of phlorizin or transfection with anti-miR-125a-5p,anti-miR-NC,miR-125a-5p mimics and negative controls.Proliferation was detected by CCK-8,and apoptosis was detected by flow cytometry.The protein expression levels of B lymphoblastoma-2 associated X protein(Bax)and B lymphocytoma-2(Bcl-2)were detected by Western blot assay.The release of lactate dehydrogenase(LDH)and the activity of superoxide dismutase(SOD)were detected by colorimetric method.Real-time fluorescence quantitative PCR(qRT-PCR)was used to detect the expression of miR-125a-5p.Results Compared with the H/R group,inhibition rate,apoptosis rate,Bax protein expression,LDH content and miR-125a-5p expression were decreased after low,medium and high doses of phlorizin treatment(P＜0.05),and SOD activity,Bcl-2 protein expression were increased(P＜0.05).After inhibiting the expression of miR-125a-5p,the inhibition rate,apoptosis rate,Bax protein expression and LDH content of H9C2 cells induced by H/R were decreased(P＜0.05),and SOD activity,Bcl-2 protein expression were increased(P＜0.05).Overexpression of miR-125a-5p reversed the effect of phloridin on H/R-induced proliferation,apoptosis and oxidative stress of H9C2 cells.Conclusion Phlorizin may reduce H/R-induced apoptosis and oxidative stress in H9C2 cells by decreasing the expression of miR-125a-5p.
