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Astragaloside-IV Protects Against Heat-induced Apoptosis by Inhibiting Excessive Activation of Mitochondrial Ca2+ Uniporter 期刊论文

编号：

2148a591-2481-42c8-88f5-bb139d771555
作者：

Dong, Zhiwei#^[1]Zhang, Chen^[3];Chen, Yajie^[1];Chen, Yu^[1];Yuan, Zhiqiang^[1];Peng, Yizhi*^[1]Cao, Tongtong(曹童童)*^[2]
语种：

英文
期刊：

CELLULAR PHYSIOLOGY AND BIOCHEMISTRY ISSN：1015-8987 2017 年 42 卷 2 期 (480 - 494)
收录：
关键词：

Astragaloside-IV Heat injury MCU Ca2+ overload ROS Apoptosis
摘要：

Background: Heat causes airway damage during inhalation injury because of bronchial epithelial cell damage. Accumulating evidence shows that mitochondrial uniporter (MCU) is involved in cell damage. We investigated the MCU activity after heat treatment and assessed whether Astragaloside-IV (AS-IV) suppresses heat-induced apoptosis in bronchial epithelial cells by inhibiting the activation of the mitochondrial Ca2+ uniporter (MCU), mitochondrial depolarisation and reactive oxygen species (ROS) production. Methods: The bronchial epithelial cell line 16HBE14o- was heat treated, and cell apoptosis was induced in vitro and in vivo. AS-IV was inorganically administered to Wistar rats twice a day after thermal inhalation injury, and 16HBE140- cells were treated with AS-IV after incubation at 47 degrees C for 5 min. Protein expression was determined using Western blotting and commercial kits, apoptosis with TUNEL staining, mitochondrial channel activity by patch clamp, reactive oxygen species by MitoSOXp (TM) fluorescence, ATP levels and enzyme activities by commercial kits as well as mitochondrial respiration and calcium by fluorescence. Results: AS-IV markedly inhibited heat-induced apoptosis, as indicated by the increased expression of the pro-apoptotic genes Bak, Bik and Bmf and increased expression of the apoptosis markers Bax, cleaved parp, cleaved caspase3 and cytochrome C. We found that MCU activation promoted mitochondrial Ca2+ overload, ATP depletion, mitochondrial ROS production and cytochrome c release and rapidly induced apoptosis. However, AS-IV treatment reduced excessive MCU activation and led to resistance against mitochondrial Ca2+ overload and excessive cytochrome C release; these effects were blocked by the MCU activator spermine. AS-IV treatment elevated ATP production and decreased ROS activity. Conclusions: MCU plays crucial roles in heat-induced mitochondrial apoptosis in 16HBE140- cells, suggesting a potential target for AS-IV treatment. (C) 2017 The Author(s) Published by S. Karger AG, Basel
推荐引用方式
GB/T 7714：

Dong Zhiwei,Zhang Chen,Chen Yajie, et al. Astragaloside-IV Protects Against Heat-induced Apoptosis by Inhibiting Excessive Activation of Mitochondrial Ca2+ Uniporter [J].CELLULAR PHYSIOLOGY AND BIOCHEMISTRY,2017,42(2):480-494.
APA：

Dong Zhiwei,Zhang Chen,Chen Yajie,Chen Yu,&Cao Tongtong.(2017).Astragaloside-IV Protects Against Heat-induced Apoptosis by Inhibiting Excessive Activation of Mitochondrial Ca2+ Uniporter .CELLULAR PHYSIOLOGY AND BIOCHEMISTRY,42(2):480-494.
MLA：

Dong Zhiwei, et al. "Astragaloside-IV Protects Against Heat-induced Apoptosis by Inhibiting Excessive Activation of Mitochondrial Ca2+ Uniporter" .CELLULAR PHYSIOLOGY AND BIOCHEMISTRY 42,2(2017):480-494.
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