Open AccessMicroRNA‑21 contributes to the puerarin‑induced cardioprotection via suppression of apoptosis and oxidative stress in a cell model of ischemia/reperfusion injury
Author(s) -
Huamin Xu,
Wen Pan,
Jian-feng Qian,
Feng Liu,
HaiQi Dong,
QingJun Liu
Publication year - 2019
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2019.10266
Subject(s) - puerarin , oxidative stress , superoxide dismutase , malondialdehyde , pharmacology , reactive oxygen species , apoptosis , chemistry , reperfusion injury , lactate dehydrogenase , nadph oxidase , glutathione peroxidase , viability assay , cardioprotection , biochemistry , biology , ischemia , medicine , enzyme , pathology , alternative medicine
Puerarin, a major bioactive constituent of the Radix puerariae, can ameliorate myocardial ischemia/reperfusion (I/R) injury. Emerging evidence supports that microRNA (miR)‑21 functions as a protective factor against I/R and/or hypoxia‑reperfusion (H/R)‑induced myocardial injury. However, the role of miR‑21 in the cardioprotective effect of puerarin remains unclear. Therefore, the purpose of the present study was to demonstrate the involvement of miR‑21 in the cardioprotective mechanisms of puerarin using a cell model of I/R injury, generated by culturing rat H9c2 cardiomyocytes under H/R conditions. The results demonstrated that pre‑treatment with puerarin significantly increased cell viability, decreased lactate dehydrogenase activity and upregulated miR‑21 expression in H/R‑treated H9c2 cells. Transfection of an miR‑21 inhibitor led to an increase in H/R‑induced cytotoxicity and reversed the protective effects of puerarin. Additionally, miR‑21 inhibition attenuated the puerarin‑induced decrease in the rate of apoptosis, caspase‑3 activity and the expression of apoptosis regulator Bax, and increased apoptosis regulator Bcl‑2 expression, under H/R conditions. Furthermore, puerarin mitigated H/R‑induced oxidative stress as evidenced by the decrease in endogenous reactive oxygen species production, malondialdehyde content and NADPH oxidase 2 expression, and enhanced the antioxidative defense system as illustrated by the increase in superoxide dismutase activity, catalase and glutathione peroxidase levels. These effects were all eliminated by miR‑21 inhibitor transfection. Furthermore, the miR‑21 inhibitor exacerbated the H/R‑induced oxidative stress and attenuated the antioxidative defense system in H/R‑treated H9c2 cells. Taken together, the results suggested that miR‑21 mediated the cardioprotective effects of puerarin against myocardial H/R injury by inhibiting apoptosis and oxidative stress.