Protective effects of cerium oxide on ibuprofen-induced renal injury in rats with ureteral obstruction.

Abstract

Background: Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used for pain management, but they can cause nephrotoxicity, particularly in patients with existing renal impairment. Cerium oxide (CeO₂), an antioxidant nanoparticle, may provide protection against renal damage caused by NSAIDs.

Aim: To assess the protective effects of CeO₂ against ibuprofen-induced renal injury in a rat model of unilateral ureteral obstruction (UUO).

Methods: Thirty male Wistar albino rats, weighing between 300 g and 425 g, were randomly divided into five groups (n = 6 each): Control (sham), UUO only, UUO + ibuprofen, UUO + ibuprofen + CeO₂, and UUO + CeO₂. UUO was surgically induced in all groups except the control group. Treatments were administered for a duration of 21 days. Serum levels of blood urea nitrogen, creatinine, malondialdehyde, and nitric oxide were measured. In addition, histopathological analysis was performed on both kidneys to assess parameters such as glomerular vacuolization (GV), tubular dilation, vascular hypertrophy, tubular necrosis, Bowman's space dilation, hyaline casts, lymphocyte infiltration, and tubular desquamation.

Results: In the right (non-obstructed) kidneys, the UUO + CeO₂ group exhibited significantly lower levels of GV, tubular hyaline casts, and tubular desquamation compared to the UUO + ibuprofen group (P < 0.05). In the left (obstructed) kidneys, the CeO₂-treated group also exhibited significant reductions in GV, vascular hypertrophy, and tubular hyaline casts (P < 0.05). Furthermore, malondialdehyde levels were markedly decreased in the CeO₂ groups, whereas nitric oxide levels were elevated in the ibuprofen group. Blood urea nitrogen and creatinine levels increased across all UUO groups, but no significant differences were observed between the treatment groups.

Conclusion: CeO₂ attenuates ibuprofen-induced renal injury in rats with UUO, likely through antioxidative mechanisms. These findings suggest that CeO₂ could serve as a potential nephroprotective adjunct during NSAID therapy in patients with obstructive renal conditions.