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Ginsenoside Rg1 Protects Cardiomyocytes Against Hypoxia/Reoxygenation Injury via Activation of Nrf2/HO-1 Signaling and Inhibition of JNK
Author(s) -
Qianhui Li,
Xin Yin,
Yu Chen,
Yong Tang,
Yachen Zhang
Publication year - 2017
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000484578
Subject(s) - reactive oxygen species , chemistry , ginsenoside , oxidative stress , pharmacology , cardioprotection , glutathione , apoptosis , superoxide dismutase , ginsenoside rg1 , mapk/erk pathway , antioxidant , glutathione peroxidase , ginseng , heme oxygenase , intracellular , signal transduction , microbiology and biotechnology , biochemistry , biology , heme , medicine , enzyme , ischemia , alternative medicine , pathology
Excessive reactive oxygen species (ROS) disturb the physiology of H9c2 cells, which is regarded as a major cause of H9c2 cardiomyocyte apoptosis. Ginsenoside Rg1 is the main active extract of ginseng, which has important antioxidant properties in various cell models. This project investigated the role of ginsenoside Rg1 in hypoxia/reoxygenation (H/R)-induced oxidative stress injury in cultured H9c2 cells to reveal the underlying signaling pathways.

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