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Myricetin protects against H 2 O 2 ‐induced oxidative damage and apoptosis in bovine mammary epithelial cells
Author(s) -
Kan Xingchi,
Liu Juxiong,
Chen Yingsheng,
Guo Wenjin,
Xu Dianwen,
Cheng Ji,
Cao Yu,
Yang Zhanqing,
Fu Shoupeng
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.30035
Subject(s) - oxidative stress , reactive oxygen species , malondialdehyde , apoptosis , superoxide dismutase , ampk , chemistry , oxidative phosphorylation , myr , microbiology and biotechnology , biochemistry , biology , kinase , protein kinase a , genome , gene
High‐producing dairy cows are prone to oxidative stress due to their high secretion and strong metabolism, and excessive oxidative stress may cause the apoptosis of bovine mammary epithelial cells (bMECs). Myricetin (Myr) has been shown to have a wide range of pharmaceutical activities. The aim of this study was to evaluate the effect of Myr on hydrogen peroxide (H 2 O 2 )‐induced oxidative stress and apoptosis in bMECs and to clarify the underlying mechanism. bMECs were pretreated with or without Myr and then stimulated with H 2 O 2 . The results showed that Myr significantly increased the total antioxidant capacity and superoxide dismutase levels and decreased the malondialdehyde (MDA) and reactive oxygen species (ROS) levels in a model of oxidative stress induced by H 2 O 2 in bMECs. Mechanistic studies found that Myr inhibited H 2 O 2 ‐induced oxidative stress in bMECs through the adenosine monophosphate‐activated protein kinase/nuclear factor erythroid‐2 related factor 2 (AMPK/NRF2) signaling pathway. Additional research found that Myr could also inhibit H 2 O 2 ‐induced apoptosis in bMECs through NRF2. These data suggest that Myr effectively alleviated oxidative stress and apoptosis in H 2 O 2 ‐induced bMECs through the activation of the AMPK/NRF2 signaling pathway.