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Ginsenoside Rg1 protects H9c2 cells against nutritional stress‐induced injury via aldolase /AMPK/PINK1 signalling
Author(s) -
Xu ZhiMeng,
Li ChengBin,
Liu QingLing,
Yang Hua,
Li Ping
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29150
Subject(s) - ampk , pink1 , ginsenoside rg1 , chemistry , microbiology and biotechnology , aldolase a , kinase , ginsenoside , protein kinase a , apoptosis , biochemistry , biology , medicine , autophagy , enzyme , ginseng , mitophagy , alternative medicine , pathology
Insufficient nutrients supply will greatly affect the function of cardiac myocytes. The adaptive responses of cardiac myocytes to nutritional stress are not fully known. Ginsenoside Rg1 is one of the most pharmacologically active components in Panax Ginseng and possesses protective effects on cardiomyocyte. Here, we investigate the effects of ginsenoside Rg1 on H9c2 cells which were subjected to nutritional stress. Nutritional stress‐induced by glucose deprivation strongly induced cell death and this response was inhibited by ginsenoside Rg1. Importantly, glucose deprivation decreased intracellular ATP levels and mitochondrial membrane potential. Ginsenoside Rg1 rescued ATP levels and mitochondrial membrane potential in nutrient‐starved cells. For molecular mechanisms, ginsenoside Rg1 increased the expressions of PTEN‐induced kinase 1 (PINK1) and p‐AMPK in glucose deprivation treated H9c2 cells. Reducing the expression of aldolase in H9c2 cells inhibited ginsenoside Rg1′s actions on PINK1 and p‐AMPK. Further, the nutritional stress mice were used to verify the mechanisms obtained in vitro. Ginsenoside Rg1 increased the expressions of aldolase, p‐AMPK, and PINK1 in starved mice heart. Taken together, our results reveal that ginsenoside Rg1 limits nutritional stress‐induced H9c2 cells injury by regulating the aldolase /AMP‐activated protein kinase/PINK1 pathway.