宫内窘迫后胎鼠肾脏细胞间粘附分子-1的表达及意义

Expression of intercelluar adhesion molecule-1 in the fetal kidneys of rats after intrauterine acute ischemia and hypoxia

摘要:

目的 缺血缺氧性肾损伤的发生过程有炎症反应参与 ,而这种炎症反应的发生与细胞粘附分子有关 ,其中细胞间粘附分子 1(ICAM 1)可上游调节并介导白细胞与内皮细胞的粘附而致肾损伤。该文旨在探讨宫内急性缺血缺氧及再灌注时ICAM 1在胎鼠肾脏炎症反应发生中的作用。方法 通过钳夹孕 2 1日龄大鼠供应子宫的血管制备胎鼠宫内不同程度缺血缺氧模型和再灌注不同时间模型 ;利用免疫组织化学技术动态观察ICAM 1的变化 ,同时应用HE染色观察病理学改变。结果 ICAM 1在假手术组胎鼠肾组织即有少量表达 ,表达部位主要在近曲小管。比较肾皮质近曲小管ICAM 1的表达情况显示 :宫内缺血缺氧后 ,在 35min和 4 5min表达增强 ,差异有显著性 (P <0 .0 5 )。与假手术组相比 ,宫内缺血缺氧 15min后再灌注 2h ,ICAM 1表达即明显增强 (P <0 .0 1) ,15h达高峰 ,再灌注 30h时表达仍强于假手术组 (P <0 .0 5 )。病理学改变 :缺血 15min再灌注 15h病理改变最明显 ,肾组织普遍充血和渗出 ,可见中性粒细胞浸润 ,肾小管普遍空泡变性 ,伴细胞核模糊 ,细胞崩解 ,基底膜阶段性断裂 ,尤以近曲小管明显。结论 宫内急性缺血和再灌注后胎肾存在炎症反应 ;宫内急性缺血缺氧可以导致ICAM 1表达增强 ,其表达变化与病理学改变一致 ,提示ICAM 1

Abstract:

Objective Some research has shown that the inflammatory reaction induced by the intercellular adhesion molecule may be involed in ischemic renal injury. Intercellular adhesion molecule-1 (ICAM-1) plays an important role in renal injury by up-regulating and inducing the adhesion between white blood cells and endothelium. This paper aims to study the effect of ICAM-1 on the inflammatory reaction in the fetal rat kidneys after acute ischemia. Methods The models of intrauterine ischemia and reperfusion in various time points were established by clamping one side of the vessels supplying blood to uterus in 21-gestational day-old Wister rats. The dynamic changes of ICAM-1 in the fetal kidneys were detected by immunohistochemical technique. Meanwhile, renal histopathological changes were observed. Another group of rats, the Sham-operation group, were given a normal blood supplement in the other side of the uterus. Results There was a small quantity expression of ICAM-1 in the cortical tubuli, especially in the proximal tubuli, in the Sham-operation group. The ICAM-1 expression began to increase 35 and 45 minutes after ischemia (P< 0.05). Compared with that of the Sham-opereation group, after a 15-minute ischemia and then a 2-hr repefusion, it began to rise (P< 0.01), reached a peak at 15 hrs of reperfusion (P< 0.01) and remained a higher level till 30 hrs of reperfusion (P< 0.05). Histological changes were most prominent after a 15-minute ischemia and then a 15-hr reperfusion, including vascular congestion, tubular vacuolar degeneration or necrosis and neutrophil accumulation. Conclusions There may be an inflammatory reaction in renal injury induced by intrauterine ischemia and reperfusion. Ischemia and reperfusion can induce the elevation of ICAM-1 expression. This suggests that ICAM-1 may play an important role in the development of inflammatory reaction in renal injury induced by acute ischemia and hypoxia.