CAJ | 학술논문

目的：观察叉头框蛋白 FoxO3a 激活 Fas 配体 FasL 介导肾缺血再灌注损伤诱导肾小管上皮细胞凋亡的作用及机制。方法双侧夹闭大鼠肾蒂缺血45 min 后再灌注建立动物模型。免疫印迹分析 FoxO3a、FasL 的表达变化；原位缺口末端标记法检测大鼠肾小管上皮细胞凋亡情况；透射电镜观察肾小管上皮细胞凋亡的超微结构变化；生化全自动分析仪检测大鼠肾功能。结果大鼠肾缺血再灌注1 h 后，FoxO3a 及 FasL 蛋白表达水平明显增加；再灌注48 h，肾小管上皮细胞凋亡损伤加剧，凋亡数目明显增加，血肌酐及尿素氮水平明显升高，与假手术组相比，差异有统计学意义（P ＜0．05，P ＜0．01）。结论大鼠肾缺血再灌注能诱导 FoxO3a 激活，进而上调 FasL 的表达，促进肾小管上皮细胞凋亡，加剧肾组织损伤。
목적：관찰차두광단백 FoxO3a 격활 Fas 배체 FasL 개도신결혈재관주손상유도신소관상피세포조망적작용급궤제。방법쌍측협폐대서신체결혈45 min 후재관주건립동물모형。면역인적분석 FoxO3a、FasL 적표체변화；원위결구말단표기법검측대서신소관상피세포조망정황；투사전경관찰신소관상피세포조망적초미결구변화；생화전자동분석의검측대서신공능。결과대서신결혈재관주1 h 후，FoxO3a 급 FasL 단백표체수평명현증가；재관주48 h，신소관상피세포조망손상가극，조망수목명현증가，혈기항급뇨소담수평명현승고，여가수술조상비，차이유통계학의의（P ＜0．05，P ＜0．01）。결론대서신결혈재관주능유도 FoxO3a 격활，진이상조 FasL 적표체，촉진신소관상피세포조망，가극신조직손상。
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.