细胞核因子kappa B p50蛋白在肾缺血再灌注损伤中的表达及意义

Expression of Nuclear factor kappa B p50 protein and its significance in renal ischemia-reperfusion injury.

目的观察大鼠肾缺血再灌注后细胞核因子Kappa B p50(Nuclear factor kappa B p50,NF-κBp50)蛋白的表达情况,探讨其参与肾缺血再灌注损伤的作用机制。方法 SD雄性大鼠48只随机分为对照组(Control组,简称C组),缺血再灌注组(Ischemia-reperfusion组,简称Ir组)两个实验组,每组各4个时相(6、12、24、72h)。采用切除右肾,夹闭左肾动脉45min后恢复灌流建立肾缺血再灌注损伤模型。观察肾组织病理变化,免疫组化二步法检测大鼠肾组织中NF-κBp50蛋白的表达情况,测定髓过氧化物酶(Mpo)活性及血清肌酐(Scr)水平以反映中性粒细胞活化及肾功能损害的程度。结果 C组大鼠肾组织形态结构正常,NF-κBp50蛋白几乎无表达;Ir组大鼠肾小管上皮细胞可见不同程度的损伤及炎细胞浸润,NF-κBp50蛋白高表达(P<0.01)。与C组比较,Ir组血清肌酐(Scr)水平明显升高,髓过氧化物酶(Mpo)活性显著增加(P<0.01)。结论缺血再灌注后肾组织中NF-κBp50蛋白表达增强,提示NF-κBp50蛋白可能在肾缺血再灌注损伤中扮演了重要角色。

Objective To investigate the expression of Nuclear factor kappa B p50（Nuclear factor kappa B p50,NF-κBp50） protein after renal ischemia-reperfusion and study the effect of NF-κBp50 protein on renal ischemia-reperfusion injury.Methods 48 normal male Sprague-Dawley rats were randomly divided into two groups：Control group（C group） and Ischemia-reperfusion group（Ir group）.The renal ischemia-reperfusion injury model was established by clamping the left renal artery for 45 min and reperfusion for 6、12、24 and 72h,the right kidneys were removed before clamping left renal vascular.Observing pathological changes of nephridial tissue.Two-step immunohistochemical methods were used to detect the changes of expression of NF-κBp50 protein.Measuring myeloperoxidase（Mpo） activity and serum creatinine（Scr） levels,which reflected neutrophil activation and kidney dysfunction.Results In Ir group,local necrosis and inflammatory cell infiltration were found by HE staining,while similar changes were scarcely visible in C group.The myeloperoxidase（Mpo） activity and the serum creatinine（Scr） levels were increased remarkably compared with C group（P0.01）.The expression of NF-κBp50 protein was gradually increased with duration of ischemia-reperfusion（P 0.01）.Conclusion The increasing expression of NF-κBp50 protein suggested that it might play important roles in renal ischemia-reperfusion injury.