NGAL 在大鼠肾脏缺血再灌注损伤不同时段中的表达及意义简

目的 探讨大鼠肾脏缺血再灌注损伤不同时段中中性粒细胞明胶酶相关脂质运载蛋白（NGAL）表达在急性肾损伤中的意义.方法 建立大鼠肾脏缺血再灌注损伤模型,46只大鼠随机分为A组和B组,各23只.观察各组肌酐、血尿素氮、β2-微球蛋白、血NGAL的变化.结果 A组血肌酐于48 h开始显著升高（P〈0.05）;尿素氮于6 h升高于48 h达高峰（P〈0.01）;β2-微球蛋白于12 h升高至48 h达高峰（P〈0.01）;NGAL于2 h开始升高,于24 h达高峰,至48 h仍高于正常（P〈0.05）;病理改变：A组大鼠受损肾小管2 h时可见刷状缘消失,管腔扩张,上皮细胞肿胀;6 h时上皮细胞有少量脱落、变性甚至坏死,可见管腔内有蛋白管型,细胞碎屑出现;12 h时可见管腔被间质水肿压迫后明显狭窄,24～48 h可见蛋白管型显著增多.结论 血NGAL可作为肾脏缺血再灌注损伤早期特异和敏感的标志物.

The expression levels of the serum NGAL in the kidney after ischemia-reperfusion injury in rats

Objective To observe the expression levels of neutrophil gelatinase - associated lipocalin （NGAL） in kidney ischemia - reperfusion injury （IRI） in rats and discuss its function in acute kidney injury. Methods Ischemia -reperfusion （IR） kidney injury rats model were established. 50 male rats were allocated into two groups randomly： sham group （group B）, IR group （group A）. To observe the changes of blood urea nitrogen （BUN）, serum creatinine （SCr）, NGAL and 132 -microglobulin in each group. The pathology demonstrated that in model group there were a loss of brush border membranes, tubular dilation and luminal debris, and the protein cast increased gradually. Results A sig- nificant rise in serum creatinine started 48 h group A （ P 〈 0.05 ） ; Urea nitrogen in 6 h rise in 48 h peak （ P 〈 0.01 ） ; Beta 2 - microglobulin peaked at 12 h increased to 48 h （ P 〈 0.01 ） ; NGAL began rising in 2 h, 24 h peak, to 48 h is still higher than normal （ P 〈 0.05 ）. Pathologi- cal changes： A group of rats impaired renal tubular 2 h visible brush border disappear, when the tube cavity expansion, swelling in the epithelial cells; 6 h epithelial ceils, degeneration and necrosis, a small amount of visible type pipe cavity contains protein, cell debris; 12 h visible lumen is interstitial edema after compression obviously narrow, 24 -48 h visible tube type protein increased significantly. Conclusion NGAL may re- present an early, sensitive and specific serum biomarker for ischemic -reperfusion renal injury.