Effect and its mechanism of FoxO3a activates FasL on renal tubular epithelial cell apoptosis induced by renal ischemia/reperfusion injury
10.13699/j.cnki.1001-6821.2014.10.018
- VernacularTitle:FoxO3a 激活 FasL 介导肾缺血再灌注中肾小管上皮细胞凋亡的作用及机制
- Author:
Jian XU
1
;
Yan WANG
;
Huai-Xue JI
;
Shu-Qun HU
;
Hong-Yan DONG
;
Ling REN
Author Information
1. 徐州医学院 附属医院 药剂科
- Keywords:
forkhead box proteinO3a;
Fas ligand;
ischemia /reperfu-sion;
renal tubular epithelial cell;
apoptosis
- From:
The Chinese Journal of Clinical Pharmacology
2014;(10):929-931
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the role and mechanism of forkhead box proteinO3a activates Fas ligand on renal tubular epithelial cell ( RTC ) apoptosis induced by renal ischemia /reperfusion ( I/R ) . Methods The model by clamping renal pedicles for 45 minutes follow-ing reperfusion was established.The protein expression of forkhead box proteinO3a and Fas ligand were examined by western blotting.Apoptosis of RTC was assessed by TdT -mediated dUTP nick -end Labeling (TUNEL) method and transmission electron microscopic (TEM).Renal function was assessed by biochemical automatic analyzer .Results The protein expression level of forkhead box proteinO 3a and Fas ligand was increased significantly following renal I /R at 1 h.RTC nucleus was shrinking, crushing followed renal I /R, and a significant increase in the number of TUNEL -positive cells following renal I /R was displayed com-pared with the sham group.The level of blood urea nitrogen(BUN) and serum creatinine ( Scr) was increased significantly compared with the sham group (P <0.05,P <0.01).Conclusion FoxO3a could be acti-vated during renal I /R, and then up -regulated FasL protein expression , facilitated renal tubular epithelial cell apoptosis , in turn, aggravated renal I /R injury in rats.
