A Role for HO-1 in Renal Function Impairment in Animals Subjected to Ischemic and Reperfusion Injury and Treated With Immunosuppressive Drugs

Autor: M.A. dos Reis, P.W. Wang, Marcos Antonio Cenedeze, Carla Q. Feitoza, Alvaro Pacheco-Silva, Niels Olsen Saraiva Câmara, Giselle Martins Gonçalves, V.P.A. Teixeira, Ana Paula Fernandes Bertocchi, M.J. Damião
Rok vydání: 2007
Předmět:
Zdroj: Transplantation Proceedings. 39:424-426
ISSN: 0041-1345
Popis: Introduction Ischemia/reperfusion injury (IRI) represents the single major antigen-independent factor implicated in pathogenesis of chronic graft dysfunction. Tacrolimus is a calcineurin inhibitor, which has been suggested to be helpful in cyclosporine-related chronic toxicity. Rapamycin has antiproliferative properties that may impair renal regeneration after IRI. Therefore, immunosuppressive drugs might impair renal graft outcome in those organs suffering IRI. Material and Methods C57B1/6 male mice subjected to 45 minutes of renal pedicle ligation were reperfused for 24 hours. Mice were treated with rapamycin, cyclosporine, or tacrolimus. Blood and renal tissue samples were collected at 24 hours after IRI. Urea levels were measured. Heme Oxygenase 1 (HO-1) gene transcript was amplified by a real-time polymerase chain reaction technique. Results Animals treated with cyclosporine and subjected to IRI showed impaired renal function that peaked at 24 hours. Additional pretreatment with rapamycin produced even more impairment of renal function, when compared with controls. However, tacrolimus pretreatment was associated with a better renal outcome. HO-1 expression was upregulated after IRI by 2.6 arbitrary units at 24 hours. Rapamycin showed worse impairment of renal function. Conclusion Tacrolimus was not associated with worsening renal function when compared with animals just subjected to IRI. Upregulation of HO-1 may be an attractive approach to limit graft injury.
Databáze: OpenAIRE