@article{APS5383,
author = {Hong-liang Kong and Zhan-quan Li and Ying-jun Zhao and Shu-mei Zhao and Li Zhu and Tong Li and Yao Fu and Hui-jun Li},
title = {Ginsenoside Rb1 protects cardiomyocytes against CoCl2-induced apoptosis in neonatal rats by inhibiting mitochondria permeability transition pore opening},
journal = {Acta Pharmacologica Sinica},
volume = {31},
number = {6},
year = {2016},
keywords = {},
abstract = {Aim: To investigate whether mitochondria permeability transition pore (mPTP) opening was involved in ginsenoside Rb1 (Gs-Rb1) induced anti-hypoxia effects in neonatal rat cardiomyocytes ex vivo.
Methods: Cardiomyocytes were randomly divided into 7 groups: control group, hypoxia group (500 μmol/L CoCl2), Gs-Rb1 200 μmol/L group (CoCl2 intervention+Gs-Rb1), wortmannin (PI3K inhibitor) 0.5 μmol/L group, wortmannin+Gs-Rb1 group, adenine 9-β-D-arabinofuranoside (Ara A, AMPK inhibitor) 500 μmol/L group, and Ara A and Gs-Rb1 group. Apoptosis rate was determined by using flow cytometry. The opening of the transient mPTP was assessed by using co-loading with calcein AM and CoCl2 in high conductance mode. Expression of GSK-3β, cytochrome c, caspase-3 and poly (ADP-ribose) polymerase (PARP) was measured by using Western blotting. ΔGSK-3β was defined as the ratio of p-Ser9-GSK-3β to total GSK-3β.
Results: CoCl2 significantly stimulated mPTP opening and up-regulated the level of ΔGSK-3β. There was a statistically significant positive correlation between apoptosis rate and mPTP opening, between apoptosis rate and ΔGSK-3β, and between mPTP opening and ΔGSK-3β. Gs-Rb1 significantly inhibited mPTP opening induced by hypoxia (41.3%±2.0%, P},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/5383}
}