GW24-e1021 Puerarin prevents oxidative stress-induced mitochondrial damage via inhibiting GSK-3β activity. (1st October 2013)

• Record Type: Journal Article
• Authors: Jingman, Xu; Xu, Jingman; Cui, Shuxia; Li, Ning; Xiong, Ruiyuan; Tian, Wei; Tian, Wei
• Is Part Of: Heart. Volume 99(2013)Supplement 3
• Page Start: A57
• Page End: A57
• Publication Date: 2013-10-01
• Subjects: Heart -- Diseases -- Treatment -- Periodicals; Cardiology -- Periodicals; 616.12
• DOI: 10.1136/heartjnl-2013-304613.157
• Languages: English
• ISSNs: 1355-6037

Abstract

Abstract : Objectives: Glycogen synthesis kinase-3β (GSK-3 β ) has been widely proved to be linked to the inhibition of the mPTP opening. This study aimed to determine whether puerarin prevents oxidative stress-induced mitochondrial damage via inhibiting GSK-3β activity. Methods: Cardiac H9c2 cells were exposed to H2 O2 for 20 min to induce mitochondrial oxidative damage. Mitochondrial membrane potential (ΔΨm) was measured by staining cells with tetramethylrhodamine ethyl ester (TMRE). V-akt-murinet hymoma viral onco-gene homolog (Akt), and GSK-3 β phosphorylation were measured with Western blotting. Results: Treatment of cardiac cells with puerarin prevented H2 O2 -induced loss of ΔΨm suggesting that puerarin prevents oxidative stress-induced mitochondrial damage. Puerarin did not alter the Aktphosphorylation, indicating that Aktmay not be involved in the cardioprotective effect of puerarin. However, treatment of cardiac cells with puerarin significantly increased GSK-3β phosphorylation, indicating that puerarin may prevent oxidative stress-induced myocardial injury through downregulating GSK-3β activity. Conclusions: Puerarin prevents oxidative stress-induced mitochondrial damage via inhibiting GSK-3β activity.