Multi-Targeted Anti-Gout Effects of Anthocleista nobilis, a Traditional West African Medicinal Plant: Urate-Lowering and Anti-Inflammatory Actions in a Composite Mouse Model.

ETHNOPHARMACOLOGICAL RELEVANCE Anthocleista nobilis, a West African medicinal plant, has traditionally been used for rheumatism, arthritis, pain, inflammatory conditions, and metabolic disorders. However, direct ethnobotanical evidence for its traditional use specifically against gout is limited. The present study therefore pharmacologically explored the potential of A. nobilis ethanolic extract (ANEE) in gout-related experimental models.

Aim

OF THE STUDY This study aimed to characterize the phytochemical and safety profiles of A. nobilis ethanolic extract (ANEE) and evaluate its pharmacological effects and potential mechanisms.

Materials And Methods

Phytochemical constituents were tentatively annotated by HPLC-QTOF-MS. Acute and 13-week repeated-dose toxicity studies were conducted in ICR mice. A murine composite gout model, combining potassium oxonate/hypoxanthine-induced hyperuricemia and intra-articular monosodium urate (MSU) crystal injection, was established. ANEE (200, 400, 800 mg/kg) was orally administered. Plasma uric acid (UA), hepatic xanthine oxidase (XOD), renal pro-inflammatory cytokines, and histopathology were evaluated.

Results

Several constituents, including linoleic acid and palmitic acid, were tentatively annotated by HPLC-QTOF-MS. No mortality or apparent acute toxicity was observed following a single administration of 200 mg ANEE per mouse, corresponding nominally to approximately 8,000 mg/kg based on an average body weight of 25 g. In the gout model, high-dose ANEE (800 mg/kg) significantly decreased plasma UA by 63.4%, inhibited hepatic XOD, and reduced joint edema by 45.4% at 144 h. It also downregulated renal IL-1β, IL-6, and TNF-α by 33.4%, 40.3%, and 20.7%, respectively. Histopathology confirmed alleviated synovial inflammation and renal tubular injury.

Conclusion

ANEE exhibited urate-lowering and anti-inflammatory effects in the composite gout model, while the in vitro and in vivo findings suggest that XOD inhibition may contribute to its urate-lowering activity. No major treatment-related abnormalities were observed under the toxicity conditions examined. These findings support further pharmacological investigation of ANEE in gout-related models.