PT  - JOURNAL ARTICLE
AU  - Zhouqing, Huang
AU  - Bozhi, Ye
AU  - Weijian, Huang
TI  - GW24-e1352 Berberine mitigated cardiac hypoxiareoxygenation injury by Suppressed Autophagy and Reduced Cell Death via inhibition of the activation of AMPK-mTOR signalling pathway in rat H9c2 cells
AID  - 10.1136/heartjnl-2013-304613.253
DP  - 2013 Aug 01
TA  - Heart
PG  - A93--A93
VI  - 99
IP  - Suppl 3
4099  - http://heart.bmj.com/content/99/Suppl_3/A93.2.short
4100  - http://heart.bmj.com/content/99/Suppl_3/A93.2.full
SO  - Heart2013 Aug 01; 99
AB  - Objectives The present study was designed to investigate the effect of berberine on the autophagy level in rat H9c2 myocytes undergoing hypoxia/reoxygenation (H/R) injury and the mechanism involved in the process. Methods H9c2 myocytes was cultured in DMEM without glucose and fetal bovine serum and subjected to H/R. The cell viability was assessed by MTT assay and the activity of autophagy was detected by electron microscopy and its component LC3-II. Western blotting was used to evaluate the expression level of AMPK, mTOR (Ser2481), SIRT1, BNIP3, and Beclin-1. Results Autophagy level greatly upregulated in H9c2 myocytes during H/R, correlated with reduced cell survival. Berberine treatment significantly enhanced the H/R-induced cell viability and inhibited the cellular autophagy level through decreasing the expression of autophagy-related proteins such as SIRT1, BNIP3 and Beclin-1. In addition, we found that the phosphorylation of AMPK and the mammalian target of rapamycin (mTOR) at Ser2481 was increased during H/R in myocytes and both were attenuated by berberine. Conclusions Berberine play its beneficial effects by decreasing the level of autophagy in H9c2 myocytes during H/R injury through suppressing the activation of AMPK-mTOR pathway and the expression of SIRT1, BNIP3 and Beclin-1.