摘要
目的探讨白细胞的粘附在初发期急性肾小管坏死(ATN)的病理生理学过程中所起的作用。方法Wistar雄性大鼠32只,随机分为4组。肌肉注射甘油制作ATN动物模型,应用细胞间粘附分子-1单抗防治初发期大鼠ATN,观察其肾脏病理学及血尿素氮和血肌酐变化。结果给药24 h后治疗组血肌酐值[(412.31±94.42)μmol/L]明显低于CD3对照组血肌酐[(990.21±171.25)μmol/L](P<0.05)。模型组与CD3对照组可见明显肾小管坏死,而治疗组仅2例出现较轻的坏死灶。结论白细胞的粘附在ATN发病过程中具有重要作用,应用细胞间粘附分子-1单抗阻断白细胞的粘附能明显减轻肾脏病理改变。
Objective To explore the role of leukocyte adhesion in the pathophysiology of glycerol-induced acute renal tubular necrosis (ATN). Methods Rat models of ATN were established by intramuscular injection of glycerol in 24 Wistar rats, which were divided randomly into 3 groups of equal number according to the agents coinjected with glycerol for the prevention of ATN, with another 8 rats serving as normal control. One of the 3 groups received a monoclonal antibody (mAb) against intercellualr adhesion molecule-1 (anti-ICAM-1) and another received CD3 mAb, leaving one group untreated. Both functional impairment and histological changes in the rats were observed. Results Plasma creatinine measured 24 h after the injection of glycerol was 412.31±94.42 μmol/L in rats treated with anti-ICAM-1, significantly lower than that in CD3 mAb-treated rats (990.21±171.25 μmol/L, P<0.05). Moderate to severe necrosis in the outer renal medulla with frequent mitoses was present in rats with ATN receiving CD3 mAB or nothing, but only mild necrosis with few mitoses occurred in merely 2 of those rats with anti-ICAM-1 treatment. Conclusion Leukocytes and adhesion molecules play critical roles in the pathophysiology of glycerol-induced ATN, and anti-ICAM-1 which blocks the adhesion of the leukocytes may alleviate the pathological changes in the kidney.
出处
《第一军医大学学报》
CSCD
北大核心
2002年第8期748-750,共3页
Journal of First Military Medical University
关键词
粘附分子
单克隆抗体
急性肾小管坏死
adhesion molecule
monoclonal antibody
renal tubular necrosis
