Renoprotective potency of heme oxygenase-1 induction in rat renal ischemia-reperfusion.
Fiche publication
Date publication
septembre 2009
Auteurs
Membres identifiés du Cancéropôle Est :
Dr ESCHWEGE Pascal
Tous les auteurs :
Chok MK, Ferlicot S, Conti M, Almolki A, Durrbach A, Loric S, Benoit G, Droupy S, Eschwege P
Lien Pubmed
Résumé
PURPOSE: Renal injury caused by ischemia-reperfusion (IR) can lead to acute renal failure or delayed graft function. Renal ischemia-reperfusion (RIR) induces inflammatory disorders via activation of arachidonic acid metabolism into prostaglandin E(2) (PGE(2)). Two inducible enzymes, COX-2 and microsomal prostaglandin E synthase (mPGES), regulate PGE(2) production. Heme oxygenase-1 (HO-1) is a cytoprotective enzyme activated during cellular stress. Overexpression of HO-1 is beneficial in transplantation models including antigen-independent IR injury, acute and chronic allograft rejection. MATERIALS AND METHODS: We investigated the effect of HO-1 induction on the COX pathway, antioxidant enzyme activities, malondialdehyde (MDA) levels, and apoptosis in rat kidneys subjected to 45 min ischemia and 1 h or 24 h reperfusion. Rats were injected intraperitoneally with either: 50 mg/kg hemin (HO-1 inducer groups: H1, H2); 50 micromol/kg ZnPP (HO-1 inhibitor groups: Hz1, Hz2); or 0.9% saline (control groups: r1, r2). Sham animals (Sh) did not undergo RIR. RESULTS: Serum creatinine increased significantly after RIR (r vs Sh; p
Référence
Inflamm Allergy Drug Targets. 2009 Sep;8(4):252-9.