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01.12.2016 | Research article | Ausgabe 1/2016 Open Access

BMC Complementary Medicine and Therapies 1/2016

Ginsenoside Rg1 protects starving H9c2 cells by dissociation of Bcl-2-Beclin1 complex

Zeitschrift:
BMC Complementary Medicine and Therapies > Ausgabe 1/2016
Autoren:
Dan Li, Jun Wang, Jincai Hou, Jianhua Fu, Dennis Chang, Alan Bensoussan, Jianxun Liu
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​s12906-016-1112-2) contains supplementary material, which is available to authorized users.

Abstract

Background

Autophagy can result in cellular adaptation, as well as cell survival or cell death. We investigated how ginsenoside Rg1(G-Rg1) regulates the relationship between autophagy and apoptosis induced by continuous starvation.

Methods

H9c2 cells under continuous starvation were treated with or without ginsenoside Rg1, and autophagy and apoptosis related proteins were assessed over a continuous time course by Western blot. Dynamic fluorescence intensity of green fluorescent protein (GFP)-LC3 was used to assess autophagosome formation by live cell imaging. Cyan fluorescent protein (CFP) -Beclin1(BECN1) and yellow fluorescent protein (YFP) -Bcl-2 were co-transfected into cells to observe ginsenoside Rg1 regulation of BECN1/Bcl-2 interaction using Fluorescence Resonance Energy Transfer (FRET). Immunoprecipitation was also used to assess BECN1/Bcl-2 interaction over a continuous time course.

Results

In H9c2 cells, starvation induced both apoptosis and autophagy. Cell apoptosis was significantly attenuated in ginsenoside Rg1-treated conditions, while autophagy was promoted. Ginsenoside Rg1 weakened the interaction between Beclin1 and Bcl-2, inhibiting apoptosis while promoting autophagy. Our results suggest that autophagy is beneficial to starved cardiac cells over a period of time. Furthermore, we describe the effect of ginsenoside Rg1 on the relationship between autophagy and apoptosis during starvation.

Conclusions

Our findings provide valuable evidence for employing ginsenoside Rg1 as a specific promoter of autophagy and inhibitor of apoptosis.
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