Ginsenoside Rg1 protects starving H9c2 cells by dissociation of Bcl-2-Beclin1 complex.
Ginsenoside Rg1 protects starving H9c2 cells by dissociation of Bcl-2-Beclin1 complex.
复制标题
DOI：
10.1186/s12906-016-1112-2
复制
发表时间：
2016-05-26
影响因子：
--
通讯作者：
Liu J
中科院分区：
文献类型：
--
作者：
Li D;Wang J;Hou J;Fu J;Chang D;Bensoussan A;Liu J
自噬可以导致细胞适应以及细胞存活或细胞死亡。我们研究了人参皂苷Rg1（G-Rg1）如何调节持续饥饿诱导的自噬和细胞凋亡之间的关系。使用或不使用人参皂苷 Rg1 处理连续饥饿下的 H9c2 细胞，并通过蛋白质印迹在连续时间过程中评估自噬和凋亡相关蛋白。绿色荧光蛋白 (GFP)-LC3 的动态荧光强度用于通过活细胞成像评估自噬体形成。将青色荧光蛋白（CFP）-Beclin1（BECN1）和黄色荧光蛋白（YFP）-Bcl-2共转染到细胞中，利用荧光共振能量转移（FRET）观察人参皂苷Rg1对BECN1/Bcl-2相互作用的调节。免疫沉淀也用于评估连续时间过程中的 BECN1/Bcl-2 相互作用。在 H9c2 细胞中，饥饿诱导细胞凋亡和自噬。在人参皂苷 Rg1 处理的条件下，细胞凋亡显着减弱，同时自噬得到促进。人参皂苷 Rg1 减弱了 Beclin1 和 Bcl-2 之间的相互作用，抑制细胞凋亡，同时促进自噬。我们的结果表明，自噬对于一段时间内饥饿的心肌细胞是有益的。此外，我们描述了人参皂苷 Rg1 对饥饿期间自噬和细胞凋亡之间关系的影响。我们的研究结果为利用人参皂苷 Rg1 作为自噬的特异性促进剂和细胞凋亡的抑制剂提供了有价值的证据。本文的在线版本 (doi:10.1186/s12906-016-1112-2) 包含补充材料，可供授权用户使用。
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. 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. 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. Our findings provide valuable evidence for employing ginsenoside Rg1 as a specific promoter of autophagy and inhibitor of apoptosis. The online version of this article (doi:10.1186/s12906-016-1112-2) contains supplementary material, which is available to authorized users.