Akanji A MurtalaOladapo E OyinloyeAdedeji F OladojaAdedeji H OlasoreLuqman O OgunjimiAkinyinka O AlabiRoyhaan O FolarinAdetola A AmballiOluwatosin O SoyinkaMuyiwa S FageyinboAbayomi S FaponleOluwatoyin O ShondeLuqmon E OsipitanJoseph O OlusolaOnaolapo R Onifade2025-07-222025-07-222025-0410.1093/rpsppr/rqaf004https://dspace.ughe.org/handle/123456789/798<jats:title>Abstract</jats:title> <jats:sec> <jats:title>Objectives</jats:title> <jats:p>This study investigated the impact of hydroethanolic leaf extract of Xylopia parviflora (XPE) on motor activities, behavioral deficits, dopamine levels, cytokine release, and oxidative radicals in rats treated with haloperidol.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>Rat groups received oral pretreatments of distilled water only (10 ml/kg; as baseline), distilled water + haloperidol (negative control), XPE at doses of 50, 100, and 200 mg/kg, and levodopa–carbidopa (25/100 mg/kg). Sixty minutes after each administration, haloperidol (2 mg/kg, i.p.) was given to all groups every other day for 21 days. Motor and behavioral functions were assessed on Day 22. Subsequently, the brains were harvested for evaluation of dopamine levels, pro-inflammatory cytokines, oxidative radicals, and histopathological examination of the striatum and substantia nigra.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>XPE improved motor impairment induced by haloperidol in rats through various mechanisms: it increased the distance covered (200 mg/kg) and reduced the number of foot slips (50–200 mg/kg) in the beam walk test, enhanced locomotor activity (200 mg/kg) in the open field test, and alleviated depression-like symptoms by decreasing immobility duration (200 mg/kg) in tail suspension test. Additionally, it counteracted haloperidol-induced dopamine depletion (100 and 200 mg/kg), suppressed tumor necrotic factor alpha (50 and 200 mg/kg), and interleukin-6(50–200 mg/kg) expressions; and reversed oxidative brain damage by increasing GSH, catalase, and decreasing MDA levels (50–200 mg/kg). XPE elicited a dose-dependent response, with low-to-moderate doses providing neuroprotection, while high doses may induce neurotoxicity.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions</jats:title> <jats:p>XPE mitigates motor dysfunction and behavioral deficits associated with Parkinson’s disease by enhancing dopamine function, inhibiting neuroinflammation, and reducing oxidative damage.</jats:p> </jats:sec>enXylopia parviforamotor dysfunctionnigrostriatal neuronscytokinesoxidative damagebehavioral deficitjournal-article