Antibodies to ICAM-1 Protect Kidneys in Severe Ischemic Reperfusion Injury
Autor: | German Ramirez, C.W. Smith, C. C. Mendiola, John R. Dietz, Hamid Rabb, Joseph V. Bonventre, Sabiha R. Saba |
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Rok vydání: | 1995 |
Předmět: |
Male
medicine.medical_specialty Neutrophils medicine.medical_treatment Biophysics Urology Ischemia Kidney Nephrectomy Biochemistry Rats Sprague-Dawley Leukocyte Count chemistry.chemical_compound Renal Artery medicine.artery medicine Animals Lymphocyte Count Renal artery Molecular Biology ICAM-1 Creatinine medicine.diagnostic_test business.industry Antibodies Monoclonal Complete blood count Cell Biology Intercellular Adhesion Molecule-1 medicine.disease Pathophysiology Rats Kidney Tubules medicine.anatomical_structure chemistry Reperfusion Injury Immunology business |
Zdroj: | Biochemical and Biophysical Research Communications. 211:67-73 |
ISSN: | 0006-291X |
Popis: | 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. |
Databáze: | OpenAIRE |
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