Astragaloside IV inhibits oxidative stress-induced mitochondrial permeability transition pore opening by inactivating GSK-3β via nitric oxide in H9c2 cardiac cells.

ABSTRACT:

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 blot. The mPTP opening was evaluated by measuring mitochondrial membrane potential (ΔΨ(m)). Nitric oxide (NO) generation was measured by 4-amino-5-methylamino-2', 7'-difluorofluorescein (DAF-FM) diacetate. Fluorescence images were obtained with confocal microscopy.

Results

Astragaloside IV significantly enhanced GSK-3β phosphorylation and prevented H(2)O(2)-induced loss of ΔΨ(m). These effects of astragaloside IV were

SUBMITTER: He Y 

PROVIDER: S-EPMC3463196 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature