Pharmacological evaluation of Hibiscus abelmoschus against scopolamine-induced amnesia and cognitive impairment in mice
2019
Astha Nigam | Mayank Kulshreshtha | Dharamveer Panjwani
Objective: Progressive loss of memory has a prominent role in devastating neurodegenerative diseases such as amnesia, dementia and Alzheimer's disease. The present study was, thus, designed to investigate the potential of Hibiscus abelmoschus (H. abelmoschus) in scopolamine-induced amnesic Swiss Albino mice. Materials and Methods: Phytochemical and acute toxicity studies of H. abelmoschus ethanolic extract (HAEE) were performed. Memory loss was induced by scopolamine (1 mg/kg, i.p), a muscarinic antagonist, and evaluated by using Morris water maze (MWM), elevated plus maze (EPM) and modified passive avoidance tests on Swiss Albino mice. Besides this, locomotor activity, serum biochemical parameters such as total cholesterol and triglyceride levels were evaluated. Lipid peroxidation (LPO), glutathione (GSH) level and catalase (CAT) activity were also checked. HAEE at a dose of 200 and 400 mg/kg body weight administered orally to the animals. Donepezil hydrochloride (1 mg/kg) was taken as standard. Results: Pre-treatment of mice with HAEE significantly reversed scopolamine-induced memory impairments, as evidenced by a significant decrease in escape latency in the MWM task, transfer latency in EPM task and an increase in step-down latency in the modified passive avoidance task. HAEE also exhibited a remarkable cholesterol and triglyceride-lowering property in the present study. Moreover, treatment with HAEE (200 and 400 mg/kg, p.o) to scopolamine-induced rats significantly decreased the LPO and increased the GSH and catalase levels. Conclusion: The memory restorative effects of H. abelmoschus in amnesia may involve its multiple functions including antioxidative and lipid-lowering properties and the presence of phytoconstituents. Thus, H. abelmoschus may act as memory enhancer and may also be useful as a supportive adjuvant in the treatment of impaired memory functions.
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