Compound K Inhibits Autophagy-Mediated Apoptosis Through Activation of the PI3K-Akt Signaling Pathway Thus Protecting Against Ischemia/Reperfusion Injury
Author(s) -
Xiangyan Li,
Qingxia Huang,
Manying Wang,
Xiuci Yan,
Xinying Song,
Rui Ma,
Rui Jiang,
Daqing Zhao,
Liwei Sun
Publication year - 2018
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 - 10.1159/000491655
Subject(s) - autophagy , pi3k/akt/mtor pathway , apoptosis , protein kinase b , viability assay , reperfusion injury , microbiology and biotechnology , signal transduction , tunel assay , reactive oxygen species , chemistry , biology , pharmacology , ischemia , biochemistry , medicine
A series of reports revealed that autophagy and apoptosis exerted detrimental effects on the pathology of cardiac ischemia/reperfusion (I/R) injury. Ginsenoside compound K (CK), a major intestinal metabolite underlying the pharmacological actions of orally administered ginseng, has a protective effect against myocardial I/R injury. However, the molecular mechanisms by which CK protects against I/R injury remain unclear. In this study, we hypothesized that the cardioprotective effects of CK against I/R injury are mediated by inhibiting autophagy/apoptosis-related signaling pathways in H9c2 cardiomyocyte cells.
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