Investigating the nitric oxide pathway stimulated by rosuvastatin on the pathological effects of renal ischemia-reperfusion in rats.

Abstract

Introduction: Renal ischemia-reperfusion (RIR) induces inflammation, oxidative stress, and impaired renal function, partly through reduced nitric oxide (NO) availability. Rosuvastatin enhances NO production and has reported organ-protective effects. This study examined whether rosuvastatin confers renoprotection in RIR through NO-dependent mechanisms.

Materials and methods: Five groups of rats (n = 6) were used: control, RIR, RIR + rosuvastatin, RIR + rosuvastatin + L-NAME (NG-Nitro-L-arginine methyl ester), and RIR + rosuvastatin + L-arginine. Drugs were administered once daily from 3 days before ischemia until 24 h after reperfusion. Twenty-four-hour urine, blood, and kidney tissues were collected for analysis. Statistical tests were performed with Prism software.

Results: Rosuvastatin significantly reduced serum urea and creatinine levels versus RIR alone. Glomerular filtration rate increased, though proteinuria remained unchanged. Inflammatory cytokines and oxidative stress decreased markedly, while tissue NO levels rose in the rosuvastatin group. L-NAME co-treatment diminished these effects, whereas L-arginine enhanced them, indicating NO involvement.

Conclusion: Rosuvastatin ameliorated renal injury in RIR, likely through activation of NO signaling. These findings suggest a potential therapeutic role for rosuvastatin in ischemic renal injury.