细胞凋亡
蛋白激酶B
LY294002型
化学
活性氧
标记法
PI3K/AKT/mTOR通路
细胞生物学
下调和上调
信号转导
生物化学
生物
基因
作者
Bin Zhang,Yaping Chen,Qiang Shen,Guiyan Liu,Jingxue Ye,Guibo Sun,Xiaobo Sun
出处
期刊:Molecules
[Multidisciplinary Digital Publishing Institute]
日期:2016-07-05
卷期号:21 (7): 880-880
被引量:51
标识
DOI:10.3390/molecules21070880
摘要
Hyperglycemia, as well as diabetes mellitus, has been shown to trigger cardiac cell apoptosis. We have previously demonstrated that myricitrin prevents endothelial cell apoptosis. However, whether myricitrin can attenuate H9c2 cell apoptosis remains unknown. In this study, we established an experiment model in H9c2 cells exposed to high glucose. We tested the hypothesis that myricitrin may inhibit high glucose (HG)-induced cardiac cell apoptosis as determined by TUNEL staining. Furthermore, myricitrin promoted antioxidative enzyme production, suppressed high glucose-induced reactive oxygen species (ROS) production and decreased mitochondrial membrane potential (MMP) in H9c2 cells. This agent significantly inhibited apoptotic protein expression, activated Akt and facilitated the transcription of NF-E2-related factor 2 (Nrf2)-mediated protein (heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO-1) expression as determined by Western blotting. Significantly, an Akt inhibitor (LY294002) or HO-1 inhibitor (ZnPP) not only inhibited myricitrin-induced HO-1/NQO-1 upregulation but also alleviated its anti-apoptotic effects. In summary, these observations demonstrate that myricitrin activates Nrf2-mediated anti-oxidant signaling and attenuates H9c2 cell apoptosis induced by high glucose via activation of Akt signaling.
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