摘要
目的:观察细胞间黏附分子1表达与大鼠肾缺血再灌注损伤的关系及红参附子提取物对其的保护作用。方法:实验于2004-03/2004-09在锦州医学院附属第一医院肾内科实验室完成。将60只雄性SD大鼠以随机数字表法分为3组,即假手术组,模型组,观察组,每组20只。对模型组,观察组大鼠采取右侧肾切除,夹闭左侧肾蒂1h,制造再灌注模型;假手术组仅切除右肾,分离左肾肾蒂但不夹闭。观察组于缺血前0.5h予红参附子提取物(参附注射液,三九雅安制药公司,批号:2003091821,20mL/支)10mL/kg门静脉注射;假手术组和模型组均注射等量生理盐水。各组分别于术后24,48h取10只大鼠处死,取肾脏标本做组织学检查,观察形态学变化,用免疫组化方法检测肾组织中细胞间黏附分子1的表达水平,并计数再灌注模型肾组织中多型核白细胞的浸润数。结果:60只大鼠全部进入结果分析。①模型组镜下可见近曲小管排列紊乱、疏松,有广泛空泡变性及片状坏死,细胞核固缩、深染。远曲小管内有大量管型形成。肾间质局部出血伴炎细胞浸润。观察组肾小管排列基本正常,小管上皮细胞轻度浊肿,偶见管型。炎细胞浸润亦较模型组明显减轻。除假手术组,各组48h改变较24h严重。②模型组肾小管Paller氏评分和肾组织中白细胞计数与假手术组比较,均显著增加(P<0.01),观察组均显著低于模型组(P<0.01)。除假手术组,各组24h与48h间差异有显著性意义(P<0.01)。③假手术组肾脏细胞间黏附分子1仅见微量表达。模型组24h出现明显细胞间黏附分子1表达,48h表达显著高于24h组(P<0.01)。观察组细胞间黏附分子1表达明显弱于模型组(P<0.01)。④再灌注24h及48h肾小管评分与肾组织中白细胞数、细胞间黏附分子1表达均呈正相关(r=0.65,0.58,P<0.05)。肾组织中白细胞数、细胞间黏附分子1表达呈正相关(r=0.85,P<0.05)。结论:细胞间黏附分子1可介导炎细胞浸润并造成肾脏缺血再灌注损伤,红参附子提取物能够抑制这种损伤过程,发挥肾保护作用。
AIM： To investigate the relationship of the expression of intercellular adhesion molecule-1 （ICAM-1） and renal ischemic reperfusion injury （IRI） in rats and the protective effect of Shenfu injection （SFI）.
METHODS： The study was done in the laboratory of Department of Nephrology, the First Affiliated Hospital of Jinzhou Medical College from March to September in 2004. We divided randomly 60 male SD rats into 3 groups： sham-operated group, I/R model group and SFI treatment group, with 20 rats in each. In sham-operated group, the rats were underwent right nephrectomy, and the left renal pedicles were separated but not occluded. In I/R model group, the rats were underwent right nephrectomy, and the left renal pedicles were occluded for 1 hour to establish ischemia. In SFI treatment group, the rats were injected with 10 mL/kg SFI from portae vein before ischemic 0.5 hour [SFI was the product of 999 Yaan Group, lot number： 2003091821, 20 mL/ampoule]. In sham-operated group and I/R model group, the rats were injected with equal 0.9% natrii chloride. At postoperative 24 hours and 48 hours, every ten rats were executed respectively for observing the morphological changes of kidney samples by histological examinations. The expression of ICAM-1 in renal tissue was assessed by immunohistochemistry method and the infiltration content of polymorphonuclear leukocytes （PMNL） was detected in rat model of renal IRI.
RESULTS： All 60 rats entered the results analysis.①In I/R model group, the proximal convoluted tubular epithelial cells arranged disorderly and loosely, accompanying vacuolar degeneration, different degrees of necrosis, pyknosis, matrix local hemorrhage and inflammatory cell infiltrations. And a large number of burettes formed in distal convoluted tubule. These changes were remarkably lightened in SFI treatment group： The renal tubules located in normal array, and the epithelial cells swelled mildly. In addition, the inflammatory cell infiltration was obviously relieved. Except sham-operated group, the changes were severer in 48-hour group than in 24-hour group.②Compared with sham-operated group, the Paller＇s grades of renal tubule and the numbers of PMNL in renal tissue were both increased obviously in I/R model group （P 〈 0.01）. And these changes were decreased in SFI treatment group then in I/R model group （P 〈 0.01）. Between each group of 24-hour and 48-hour, the changes were extremely different （P 〈 0.01） except the sham-operated group.③The ICAM-1 expressions were slight in sham-operated group, marked in I/R model group after 24 hours and increased significantly after 48 hours （P 〈 0.01）. Compared with I/R model group, ICAM-1 expressed decreasingly and conspicuously in SFI treatment group （P 〈 0.01）. ④The renal tubular Paller＇s grades were related with PMNL number and the expression of ICAM-1 positively （r=0.65, 0.58, P 〈 0.05） after reperfusion 24 hour and 48 hour, and PMNL number had a positive relationship with the expression of ICAM-1 （r=0.85, P 〈 0.05）. CONCLUSION： ICAM-1 may mediate the infiltration of inflammatory cells and contribute to renal IRI, which can be inhibited by SFI to protect the renal tissues,
出处
《中国临床康复》
CSCD
北大核心
2006年第39期126-128,共3页
Chinese Journal of Clinical Rehabilitation
