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2,3,5,4′‐Tetrahydroxystilbene‐2‐O‐β‐ d ‐glucoside eliminates ischemia/reperfusion injury–induced H9c2 cardiomyocytes apoptosis involving in Bcl‐2, Bax, caspase‐3, and Akt activation
Author(s) -
Sun Tao,
Liu Han,
Cheng Yutong,
Yan Lixiao,
Krittanawong Chayakrit,
Li Shihong,
Qian Wang,
Su Wang,
Chen Xuanzu,
Hou Xuejian,
Zhang Hongju
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.27949
Subject(s) - apoptosis , protein kinase b , chemistry , cell , reperfusion injury , microbiology and biotechnology , caspase 3 , programmed cell death , biology , ischemia , medicine , biochemistry
Objective This study was designed to explore the protective effect of 2,3,5,4′‐tetrahydroxystilbene‐2‐O‐β‐ d ‐glucoside (TSG) against ischemia/reperfusion (I/R) injury–induced cardiomyocytes apoptosis. Methods The H9c2 cell I/R injury model was induced by simultaneous shortage of nutrients and oxygen. TSG administration (0.10, 0.25, and 0.50 mM) was performed before and during I/R stimulation. Cell apoptosis was evaluated using terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Expression of cell‐related proteins was detected to assess the effect of TSG on cell apoptosis. Results I/R injury induced significant cell apoptosis. Significantly decreased Bcl‐2 and increased Bax, caspase‐3, and p‐Akt expression ( P < 0.01) was detected in the cell model of I/R injury. In contrast, TSG administration eliminated all the changes induced by I/R injury in a dose‐dependent manner. Compared with the H9c2 cell model of I/R injury, the H9c2 cells treated with 0.50 mM TSG showed the lowest cell apoptosis percentage, the highest expression of Bcl‐2, and the lowest expression of Bax, caspase‐3, and p‐Akt ( P < 0.01). Conclusion We confirmed that the protective effect of TSG against I/R injury–induced cell apoptosis in H9c2 in vitro was associated with the Bcl‐2/Bax ratio, caspase‐3, and Akt activation.