Quercetin Ameliorates Bromocriptine-induced Disruptions in Neurobehaviour and Cerebellar Histomorphology in Rats

Arojojoye Abiodun Moses¹, Tomiwa Goodness Alake¹, Ajao Joshua Aduragbemi², Akinsehinwa Akinsanmi Festus¹, Opeyemi Ojo Famuyide¹, Onaolapo Olakunle James³, Onaolapo Adejoke Yetunde⁴

1. Department of Anatomy, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria 
2. Department of Pharmacology and Therapeutics, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria 
3. Behavioural Neuroscience and Neuropharmacology Unit, Department of Pharmacology and Therapeutics, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria, ORCID: 0000-​0003-2142-6046 ojonaolapo@lautech.edu.ng  
4. Behavioural Neuroscience and Neurobiology Unit, Department of Anatomy, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria, ORCID: 0000-0001-7126-7050, ayonaolapo@lautech.edu.ng 

ABSTRACT 

Bromocriptine is a dopamine agonist commonly used in the treatment of hyperprolactinaemia and Parkinson’s disease; however, its prolonged administration has been linked to oxidative stress and neuroinflammation, particularly within the cerebellum. Quercetin, a natural flavonoid with potent antioxidant and neuroprotective properties, may counteract these effects, although its protective role against bromocriptine-induced cerebellar toxicity is not well established. This study evaluated the neurobehavioural, biochemical, and histological effects of quercetin in bromocriptine-treated rats. Sixty adult, male Wistar rats (120–150 g each) were randomly assigned into six groups (n = 10). Group A received normal saline; Groups B and C received quercetin-supplemented feed (500 and 1000 mg/kg) for 14 days. Group D was administered bromocriptine (5 mg/kg) during the second 14-day period. Groups E and F received quercetin (500 and 1000 mg/kg) concurrently with bromocriptine. Bromocriptine-treated rats (Group D) exhibited significant reductions in body weight and feed intake, while Groups E and F showed significant recovery. Open-field novelty-induced behaviours were altered in Group D, with significant reductions in line crossing and rearing, whereas these behaviours improved in quercetin-treated groups. Self-grooming increased in Group D but declined significantly in Groups E and F. Biochemical analyses indicated heightened oxidative stress and inflammation in Group D, with increased MDA and pro-inflammatory cytokines (IL-6, IL-1β, TNF-α), and reduced TAC and IL-10. Histological assessment revealed cerebellar neuronal disruption in Group D, while quercetin co-treatment preserved cerebellar architecture. In conclusion, quercetin attenuated bromocriptine-induced behavioural deficits, oxidative damage, inflammation, and changes in cerebellar histopathology; demonstrating promising neuroprotective potential. 

KEYWORDS: Ergot Alkaloid, Neurotoxicity, Neuroinflammation, Neuroprotection, Oxidative stress