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Neuregulin‐1 protects myocardial cells against H 2 O 2 ‐induced apoptosis by regulating endoplasmic reticulum stress
Author(s) -
Xu Min,
Wu Xuesi,
Jie Bingzhang,
Zhang Xiaoxia,
Zhang Jinglan,
Xin Yi,
Guo Yongfang
Publication year - 2014
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.3038
Subject(s) - endoplasmic reticulum , malondialdehyde , unfolded protein response , oxidative stress , cardioprotection , apoptosis , superoxide dismutase , lactate dehydrogenase , chop , chemistry , microbiology and biotechnology , medicine , endocrinology , biochemistry , biology , myocardial infarction , enzyme
Neuregulin‐1 (NRG‐1) is a stress‐mediated growth factor secreted by cardiovascular endothelial cells and provides the protection to myocardial cells, but the underlying mechanisms are not fully understood. This study aimed to demonstrate that NRG‐1 protects myocardial cells exposed to oxidative damage by regulating endoplasmic reticulum (ER) stress. Neonatal rat cardiac myocytes (NRCMs) were isolated and treated with H 2 O 2 as a cellular model of ER stress. NRCMs were pretreated with different concentrations of NRG‐1. We found that NRG‐1 increased the viability and reduced the apoptosis of NRCMs treated by H 2 O 2 . Moreover, NRG‐1 reduced lactate dehydrogenase level, increased superoxide dismutase activity and decreased malondialdehyde content in NRCMs treated by H 2 O 2 . Finally, we demonstrated that NRG‐1 alleviated ER stress and decreased CHOP and GRP78 protein levels in NRCMs treated by H 2 O 2 . Taken together, these data indicate that NRG‐1 relieves oxidative and ER stress in NRCMs and suggest that NRG‐1 is a promising agent for cardioprotection. Copyright © 2014 John Wiley & Sons, Ltd.