Effect of the inhibitor of the fosfodiesterase 5 and N-acetylcisteine in the ischemic acute kidney injury in rats

Abstract

Ischemic acute kidney injury (AKI) triggers a cascade of events involving inflammatory response and generation of reactive oxygen species that result in endothelial and tubular injury. Moreover, hypoxia cellular activates mechanisms of adaptation and cellular cytoprotection as the enzyme heme oxygenase-1 (HO-1). Sildenafil citrate and N-acetylcysteine (NAC) show anti-inflammatory and antioxidant properties with vascular protection. The objective of this study is to evaluate the sildenafil citrate and NAC role in different times of ischemic LRA in rats. Material and Methods: Wistar rats, adults and males (250 to 300g), divided into the following groups: SHAM (surgery simulation); Sildenafil (sildenafil 0,25 mg/kg, v.o., 1 day); NAC (NAC 300mg/kg, i.p., 1 a day); Ischemia 30 min (renal clamping for 30 min); Ischemia 45 min (clamping for 45 min); Ischemia 30 min + sildenafil; Ischemia 45 min + sildenafil; Ischemia 30 min + NAC; Isquemia 45 min + NAC. Renal function, oxidative profile, histology of renal tissue, enzyme activity of HO-1, gene expression of HO-1 and release of nitric oxide (NO) will be evaluated. (AU)