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

Bromocriptine is a dopamine agonist commonly used in the treatment of hyperprolactinaemia and Parkinson’s disease, but 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 neurobehavioral, biochemical, and histological effects of quercetin in bromocriptine-treated rats. Sixty adult, male Wistar rats (120–150 g) 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 cerebellar histopathology, demonstrating promising neuroprotective potential.