title: Iloprost downregulates expression of adhesion molecules and reduces renal injury induced by abdominal aortic ischemia-reperfusion.
abstract: The aim of this study was to examine the effect of iloprost in renal injury induced by abdominal aortic ischemia-reperfusion (IR) and how it can modulate the expression of adhesion molecules during this effect. Twenty-four Wistar-Albino rats were randomized into three groups (n=8) as follows: control (sham laparotomy), aortic IR (120 min ischemia and 120 min reperfusion), and aortic IR + iloprost (0.45 microg/kg/hr intravenous infusion during 120 min reperfusion). Blood and renal tissue samples were obtained for biochemical analysis. A histological evaluation with both hematoxylin-eosin staining and immunostaining was also done. Biochemical analyses showed that aortic IR significantly increased (p<0.05 vs. control) whereas iloprost significantly decreased (p<0.05 vs. aortic IR) plasma levels of malondialdehyde, P-selectin, intercellular adhesion molecule-1 (ICAM-I), and tissue levels of malondialdehyde and catalase. Histological evaluation with immunostaining showed that aortic IR significantly increased (p<0.05 vs. control) whereas iloprost significantly decreased (p<0.05 vs. aortic IR) the immunoreactivity of P-selectin, tumor necrosis factor-alpha, CD11b, CD18, and ICAM-1. Hematoxylin-eosin staining showed that iloprost also attenuated the morphological changes associated with aortic IR. The results of this study show that iloprost reduces renal injury induced by aortic IR in rats and downregulates expression of adhesion molecules at both the local and systemic levels after aortic IR during this protective effect.
authors.affiliation: Department of Cardiovascular Surgery, Suleyman Demirel University Medical School, Isparta, Turkey. kirisilker@yahoo.com
authors.forename: Ilker
authors.initials: I
authors.lastname: Kiris
authors.forename: Ilker
authors.initials: I
authors.lastname: Tekin
authors.forename: Nigar
authors.initials: N
authors.lastname: Yilmaz
authors.forename: Recep
authors.initials: R
authors.lastname: Sutcu
authors.forename: Nermin
authors.initials: N
authors.lastname: Karahan
authors.forename: Ahmet
authors.initials: A
authors.lastname: Ocal
mesh_terms: D000818:Animals; D001012:Aorta, Abdominal / Q000601:surgery*; D039481:CD11b Antigen / Q000378:metabolism; D018821:CD18 Antigens / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000097:blood / Q000378:metabolism*; D003250:Constriction; D004195:Disease Models, Animal; D015536:Down-Regulation; D005260:Female; D016285:Iloprost / Q000008:administration & dosage / Q000494:pharmacology*; D007262:Infusions, Intravenous; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007668:Kidney / Q000098:blood supply / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D007674:Kidney Diseases / Q000209:etiology / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D019007:P-Selectin / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000209:etiology / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014656:Vascular Surgical Procedures / Q000009:adverse effects*
chemical_list: D039481:CD11b Antigen; D018821:CD18 Antigens; D015815:Cell Adhesion Molecules; D019007:P-Selectin; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D008315:Malondialdehyde; D002374:Catalase; D016285:Iloprost