Neuroprotective and anti-parkinsonian effects of micronized purified flavonoid fraction (Daflon®) in a haloperidol-induced mouse model of Parkinsonism

Abstract

The use of haloperidol to treat mental illnesses like schizophrenia, mania, hyperactivity, and agitation is limited by its ability to cause Parkinson-like symptoms. Daflon (micronised purified flavonoid fraction) is an oral phlebotropic medication with potent antioxidant and anti-inflammatory properties. This study investigates the anti-Parkinsonian potential of Daflon in a mouse model of haloperidol-induced Parkinsonism. Thirty male mice (n=6/group) received daily treatments for seven days: Group I/control (saline, 2 mL/kg, orally), Group II (haloperidol, 2 mg/kg, intraperitoneally), Group III-IV (haloperidol 2 mg/kg, intraperitoneally + Daflon 50/100 mg/kg orally), and Group V (haloperidol 2 mg/kg, intraperitoneally + levodopa/carbidopa 10 mg/kg orally). On day 7, motor function was assessed using the catalepsy bar test. Subsequently, animals were euthanised, and brain tissues were collected to evaluate dopamine concentrations, glutamate concentrations, acetylcholinesterase (AChE) activity, and striatal histopathology. Haloperidol significantly increased cataleptic descent latency (p < 0.001), decreased dopamine concentrations (p < 0.05), and increased AChE activity (p < 0.05), while causing neuronal distortions in the striatum; glutamate concentrations remained unaffected (p > 0.05). Daflon co-treatment, particularly at 100 mg/kg, significantly shortened descent latency (p < 0.05), improved dopamine concentrations (p < 0.05), lowered AChE activity (p < 0.05), but glutamate concentration remained unaffected (p > 0.05). Histological results showed preservation of striatal neurons. Daflon exhibited neuroprotective effects comparable to levodopa/carbidopa. The findings of this study show that Daflon possesses antiparkinsonian effects against haloperidol-induced Parkinsonism.