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抗细胞间黏附分子-1抗体可保护肾脏免受严重缺血再灌注损伤。

Antibodies to ICAM-1 protect kidneys in severe ischemic reperfusion injury.

作者信息

Rabb H, Mendiola C C, Saba S R, Dietz J R, Smith C W, Bonventre J V, Ramirez G

机构信息

Department of Internal Medicine, University of South Florida, Tampa 33612, USA.

出版信息

Biochem Biophys Res Commun. 1995 Jun 6;211(1):67-73. doi: 10.1006/bbrc.1995.1779.

Abstract

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.

摘要

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。

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