Mitochondrial ROS burst as an early sign in sarsasapogenin-induced apoptosis in HepG2 cells

被引：60

作者：

Ni, Yuan ^{[1
]}

Gong, Xing-guo ^{[1
]}

Lu, Min ^{[1
]}

Chen, Han-min ^{[1
]}

Wang, Yong ^{[1
]}

机构：

[1] Zhejiang Univ, Inst Biochem, Hangzhou 310003, Zhejiang, Peoples R China

来源：

CELL BIOLOGY INTERNATIONAL | 2008年 / 32卷 / 03期

关键词：

Sarsasapogenin; Mitochondrial dysfunction; Reactive oxygen species; Cytochrome c; Apoptosis;

D O I：

10.1016/j.cellbi.2007.12.004

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 [细胞生物学]; 090102 [作物遗传育种];

摘要：

Sarsasapogenin is a steroidal sapogenin with antitumor properties. To explain the mechanism of its apoptotic effect, mitochondrial activity was assessed via a 3,(4,5- dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Flow cytometry (FCM) was used to estimate the changes in mitochondrial membrane potential (MMP), reactive oxygen species (ROS) generation, and cellular- reduced glutathione (GSH) level. Laser scanning confocal microscope (LSCM) recorded instantaneous ROS burst after application of sarsasapogenin. Western blotting was used to determine the expression level and intracellular distribution of cytochrome c (cyt c). It is demonstrated that during apoptosis, ROS burst acted as an early event followed by depolarization of MMP, prolonged ROS generation, and significantly declined GSH level. Cyt c was upregulated and released from mitochondria to cytosol during the process. These findings show that a mitochondrial ROS burst is an early upstream apoptotic signal which may trigger the mitochondrial apoptotic pathway and play a vital role in sarsasapogenin-induced HepG2 cell apoptosis. (C) 2008 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.

引用

页码：337 / 343

页数：7

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