Advanced glycation end products and its receptor induce apoptosis of L cells through NADPH oxidase mediated signaling pathway
10.3969/j.issn.1006-5725.2017.03.007
- VernacularTitle:糖基化终产物通过其受体激活NADPH氧化酶及其下游通路诱导L细胞的凋亡
- Author:
Yinghui HU
;
Zhen ZHANG
;
Lei LEI
;
Rui YANG
;
Jianghong LIN
;
Huixian ZENG
;
Hong CHEN
- Keywords:
Advanced glycation end-products;
GLUTag cells;
Apoptosis;
NADPH oxidase;
Reactive oxidative species
- From:
The Journal of Practical Medicine
2017;33(3):358-362
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of AGEs-RAGE on the apoptosis of GLUTag cells and explore the possiblc mechanism.Methods GLUTag cells treated with 0、100、200、300μg/ml of AGEs for 24h were examined for gene and protein expression of RAGE using RT-PCR and western blotting,respectively.GLUTag cells were randomly divided into four groups:control,200μg/ml AGEs,AGEs+siRNA-RAGE and AGEs+apocynin.The protein expression of p22phox、p47phox 、Bcl-2、Bax in the cells were detected with western blotting.The reactive oxygen species (ROS) levels were examined using 2'7'-dichlorodihydroflur-rescein diacetate (DCFH-DA) and the apoptosis of L cells were tested by AnnexinV-FITC/PI.Results AGEs increased thc cxpression of RAGE in a dose dependent manner.Treatment with AGEs induced a significant increase in the expression of p22phox,p47phoxand the activity of ROS,caused up-regulation of Bax and down-regulation of Bcl-2,which enhanced the apoptosis of GLUTag cells.Apocynin,the inhibitor of NADPH oxidase,prevented those responses and the effects caused by AGEs were abolished by inhibition of RAGE activity with siRNA.Conclusion AGEs positively regulate the exprcssion of NADPH oxidase-derived ROS and its down-steam signaling pathway p53/Bax by targeting RAGE,leading to the apoptosis of GLUTag cells.
