Rabb H, Mendiola C C, Saba S R, Dietz J R, Smith C W, Bonventre J V, Ramirez G
Department of Internal Medicine, University of South Florida, Tampa 33612, USA.
Biochem Biophys Res Commun. 1995 Jun 6;211(1):67-73. doi: 10.1006/bbrc.1995.1779.
ICAM-1 has been implicated in the pathophysiology of ischemic-reperfusion injury in a number of organs, but its role in mediating severe ischemic-reperfusion injury in the kidney has not been extensively studied. Uninephrectomized Sprague Dawley rats were pretreated with either control monoclonal antibody (mAb) or mAb to ICAM-1 and subjected to 60 min of renal artery occlusion. The serum creatinine, complete blood count and kidney histo-pathological damage scores (PDS) (Scale:0-4) were assessed prior to and 24 hours after ischemia. Mean serum creatinine (mg/dl) 24 hours after ischemia was significantly decreased in the anti-ICAM-1 group (1.38 +/- 0.23, p < 0.001) compared to control (2.87 +/- 0.34). PDS was also reduced in anti-ICAM-1 (2.55 +/- 0.20, p < 0.05) group compared to control (3.35 +/- 0.30). These data demonstrate that blocking ICAM-1 significantly mitigates severe ischemic acute renal failure, findings which may lead to improved therapy for this condition.
细胞间黏附分子-1（ICAM-1）已被证明与多种器官的缺血再灌注损伤病理生理过程有关，但其在介导肾脏严重缺血再灌注损伤中的作用尚未得到广泛研究。将单侧肾切除的斯普拉格-道利大鼠预先用对照单克隆抗体（mAb）或抗ICAM-1单克隆抗体处理，然后进行60分钟的肾动脉闭塞。在缺血前和缺血后24小时评估血清肌酐、全血细胞计数和肾脏组织病理学损伤评分（PDS）（范围：0-4）。与对照组（2.87±0.34）相比，抗ICAM-1组缺血后24小时的平均血清肌酐（mg/dl）显著降低（1.38±0.23，p<0.001）。与对照组（3.35±0.30）相比，抗ICAM-1组（2.55±0.20，p<0.05）的PDS也有所降低。这些数据表明，阻断ICAM-1可显著减轻严重缺血性急性肾衰竭，这一发现可能会改善对此病症的治疗。
