Integrated in vivo evaluation of the neuroprotective potential of Colocasia esculenta leaf extract in scopolamine-induced cognitive impairment and haloperidol-induced catalepsy
摘要
Aim: This experimental model assesses the neuroleptic and anti-cognitive potential of a hydroethanolic leaf extract of Colocasia esculenta (HECE) using an in vivo model.
Methodology: The study was conducted on Swiss albino mice and comprised two components: cognitive impairment and neuroleptic activity. In the cognitive model, animals were divided into control, negative control, standard, and two treatment groups receiving a hydroethanolic leaf extract of Colocasia esculenta (200 and 400 mg/kg). For neuroleptic assessment, animals were grouped into control (vehicle 10 ml/kg), standard (trihexyphenidyl 10 mg/kg + haloperidol 1 mg/kg), and two test groups receiving the extract (200 and 400 mg/kg) along with haloperidol (1 mg/kg). Behavioural evaluations were performed using the Hebb–William maze, Cook’s pole-climbing test, and haloperidol-induced catalepsy model. Biochemical and histopathological analyses were also conducted.
Results: HECE significantly ameliorate cognitive efficacy in the Hebb–William’s maze (p < 0.01), Cook’s pole-climbing test (p < 0.001), and reversing scopolamine-induced model. In both acute and chronic studies (p < 0.001), HECE produced a dose-proportional decline in haloperidol-induced catalepsy. Histopathological findings confirmed reduced neuronal degeneration, with the 400 mg/kg dose exhibiting neuroprotective efficacy comparable to that of standard drugs. All compounds were neurotoxicity-inactive (0.56–0.89), showed minimal GABA receptor interaction, and limited BBB permeability except for quercetin and dimedone; vitexin, luteolin-7-rutinoside, and orientin exhibited moderate clinical toxicity (0.51–0.52), while AChE activity was restricted to luteolin-7-rutinoside and orientin.
Conclusion: Hydro-ethanolic leaf extract of Colocasia esculenta (HECE) exhibits neurodegenerative activity and might be useful as a therapy for cognitive dysfunction disease. Furthermore, mechanism of action modulations is described for clinical applicability.
Graphic abstract