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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45min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。
OBJECTIVE: To investigate the effect and mechanism of FoxO3a activating Fas ligand FasL on renal tubular epithelial cell apoptosis induced by renal ischemia-reperfusion injury. Methods Bilateral occlusion rats with renal peduncle ischemia 45min after reperfusion animal models. Western blot analysis of FoxO3a, FasL expression changes; in situ nick end labeling method of rat renal tubular epithelial cell apoptosis; TEM observation of renal tubular epithelial cell apoptosis ultrastructure changes; automatic biochemical analyzer rat Kidney function. Results The expression of FoxO3a and FasL increased significantly after renal ischemia / reperfusion in 1 h, and the apoptosis of renal tubular epithelial cells was aggravated at 48 h after reperfusion, the number of apoptotic cells was significantly increased and the levels of serum creatinine and urea nitrogen were significantly increased , Compared with the sham operation group, the difference was statistically significant (P <0.05, P <0.01). Conclusion Renal ischemia / reperfusion can induce the activation of FoxO3a, up-regulate the expression of FasL, promote the apoptosis of renal tubular epithelial cells and exacerbate renal damage.