Jinkun Xi

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The purpose of this study was to determine whether exogenous zinc prevents cardiac reperfusion injury by targeting the mitochondrial permeability transition pore (mPTP) via glycogen synthase kinase-3beta (GSK-3beta). The treatment of cardiac H9c2 cells with ZnCl2 (10 microM) in the presence of zinc ionophore pyrithione for 20 min significantly enhanced(More)
The aim of this study was to test whether morphine prevents the mitochondrial permeability transition pore (mPTP) opening through Zn(2+) and glycogen synthase kinase 3beta (GSK-3beta). Fluorescence dyes including Newport Green Dichlorofluorescein (DCF), 4-amino-5-methylamino-2',7'-difluorofluorescein (DAF-FM), and tetramethylrhodamine ethyl ester (TMRE)(More)
OBJECTIVE Our aim was to determine if NO prevents mitochondrial oxidant damage by mobilizing intracellular free zinc (Zn(2+)). METHODS Zn(2+) levels were determined by imaging enzymatically isolated adult rat cardiomyocytes loaded with Newport Green DCF. Mitochondrial membrane potential (DeltaPsi(m)) was assessed by imaging cardiomyocytes loaded with(More)
The purpose of this study was to determine whether Zn2+ is involved in endoplasmic reticulum (ER) stress inhibition-induced cardioprotection against ischemia/reperfusion (I/R) injury by modulation of the mitochondrial permeability transition pore (mPTP) opening. Isolated rat hearts were subjected to 30-min regional ischemia followed by 2 h of reperfusion.(More)
OBJECTIVE This study aimed to investigate whether astragaloside IV modulates the mitochondrial permeability transition pore (mPTP) opening through glycogen synthase kinase 3β (GSK-3β) in H9c2 cells. METHODS H9c2 cells were exposed to astragaloside IV for 20 min. GSK-3β (Ser(9)), Akt (Ser(473)), and VASP (Ser(239)) activities were determined with western(More)
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