none 10.31254/phyto.2026.15201 BioMed Research Publishers BioMed Research Publishers 16195 193583303 316921 20260420131520875 10.31254 2026-04-20T13:15:26Z 2026-04-20T13:15:26Z 0 The Journal of Phytopharmacology J Phytopharmacol 2320480X 10.31254/phyto https://phytopharmajournal.com/ 04 17 2026 15 2 Omorede Ikponmwosa-Eweka https://orcid.org/0000-0002-7654-5635 Ikenna Chukwuemeka Maduako https://orcid.org/0000-0002-1001-4866 Background: Arsenic is a persistent environmental contaminant that poses a serious public health risk due to its well-documented hepatotoxic and nephrotoxic properties. Exposure to sodium arsenite (NaAsO2), a soluble inorganic arsenical compound, induces multi-organ injury through mechanisms involving oxidative stress, NF-κB-driven inflammation, and dysregulation of the Nrf2/HO-1 antioxidant pathway. Objective: This study investigated the hepatorenal protective effects of rutin (RUT) against NaAsO2-induced hepatorenal toxicity in male rats, and sought to elucidate the underlying mechanisms with specific reference to oxidative stress, inflammatory signalling, and the Nrf2/HO-1 and NF-κB pathways. Materials and Methods: Forty male Wistar rats were randomly allocated into five groups (n = 8 per group) and treated orally for 14 days as follows: Group I, vehicle control; Group II, RUT alone (50 mg/kg); Group III, NaAsO2 alone (10 mg/kg); Group IV, NaAsO2 (10 mg/kg) + RUT (25 mg/kg); and Group V, NaAsO2 (10 mg/kg) + RUT (50 mg/kg). Hepatotoxicity and nephrotoxicity were evaluated using serum biochemical markers (ALP, ALT, urea, and creatinine), histopathological examination of liver and kidney tissues, and biochemical assessment of oxidative stress indices (MDA, RONS, NO, and GSH) and inflammatory signalling proteins (NF-κB, RANTES, and Nrf2/HO-1). Results: NaAsO2 exposure significantly impaired hepatic and renal redox homeostasis, markedly elevating lipid peroxidation (MDA), reactive oxygen and nitrogen species (RONS), nitric oxide (NO), NF-κB, and RANTES, while depleting GSH content and suppressing the Nrf2/HO-1 pathway. These biochemical perturbations were accompanied by significant histopathological alterations in both liver and kidney tissues. Co-administration of RUT dose-dependently and significantly ameliorated all these changes, suppressing NF-κB activation and its downstream pro-inflammatory targets, restoring GSH levels, and upregulating Nrf2/HO-1 expression. Histological examination confirmed that RUT markedly attenuated NaAsO2-induced structural disruption in hepatic and renal tissues. Conclusion: Rutin confers potent hepatorenal protection against NaAsO2-induced toxicity through coordinated free-radical scavenging, NF-κB-mediated suppression of inflammation, and activation of the Nrf2/HO-1 antioxidant pathway. These findings suggest that RUT represents a promising therapeutic candidate for mitigating arsenic-induced hepatorenal organ damage. 04 17 2026 117 125 1 10.31254/biomed-crossmark-policy www.biomedresearch.org false 10.31254/phyto.2026.15201 https://phytopharmajournal.com/articles/abstracts/892/year=2026&vol=15&issue=2