血清NGAL 在大鼠肾脏缺血再灌注损伤不同时段 的表达及其意义

目的:观察大鼠肾脏缺血再灌注损伤不同时段血中性粒细胞明胶酶相关脂质运载蛋白(NGAL)的表达并探讨其在急性肾脏缺血再灌注损伤中的意义.方法:建立大鼠肾脏缺血再灌注损伤模型,将50只大鼠随机分为假手术组(S组)和模型组(M组),每组分为5个亚组,包括2h、6h、12h、24h、48h,每亚组大鼠5只.观察各组血NGAL,β2-微球蛋白及血尿素氮,肌酐的变化.结果:M组血NGAL于再灌注损伤后早期(2h)即开始升高,于24h达高峰,至48h仍高于正常(P＜0.05)；β2-微球蛋白于12h升高至48h达高峰(P＜0.01)；尿素氮于6h升高于48h达高峰(P＜0.01)；而血肌酐则于48h才显著升高(P＜0.05).病理显示:M组2h时可见受损肾小管上皮细胞肿胀,管腔扩张、刷状缘消失,至6h时少量上皮细胞脱落、变性甚至坏死,管腔内可见坏死脱落的细胞碎屑,蛋白管型出现,12h时可见间质水肿压迫至管腔明显狭窄,于24h、48h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敏感的生物标志物.

The Expression and Significance of Serum NGAL during the Ischemia-Reperfusion Injury happened in Rat Kidney

Objective:To observe the expression levels of neutrophil gelatinase-associated lipocalin(NGAL) in kidney ischemiareperfusion injury(IRI) in rats and to discuss its function in acute kidney injury.Methods:Ischemia-reperfusion(IR) kidney injury rats model was established.Fifty male rats were divided into two groups randomly:sham group(group S),IR group(group M),which included 2h,6h,12h,24h,48h ssubgroups,each had 5 rats.Observed the changes of blood urea nitrogen(BUN),serum creatinine(SCr),NGAL and β2-microglobulin in each group.Results:In model group,NGAL levels were increased at an early time(2h) and peaked at the 24h samples(P<0.05),and still higher than the sham group by the 48h recovery period.The β2-microglobulin showed a significant elevation at 12h and peaked at the 48h after reperfusion(P<0.01).The expression of BUN was elevated at 6h and peak at the 48h subgroup.But the SCr was enhanced only at the 48h after injury.The pathology demonstrated that in model group there were a loss of brush border membranes,tubular dilation and tubular epithelial cell edema at the 2h subgroup,and at 6h there was a small quantity of epithelium fall off,degenerate,even necrosis,luminal debris,and the protein cast appearance.The lumens was narrowed obviously by the interstitial edema at the 12h.Then the protein cast increased gradually at the 24h and 48h.Conclusion:NGAL may represent an early,sensitive and specific serum biomarker for ischemic-reperfusion renal injury.