ABSTRACT
Emblica officinalis, commonly known as amla, is an important medicinal plant of India. Its fruits have potent antioxidant activity due to the presence of tannoids, tannins, vitamin C and flavonoids. The aim of this study was to investigate the beneficial effect of the hydroalcoholic extract of the fruits of Emblica officinalis (EO) on memory impairment in Swiss albino mice. Scopolamine (1 mg kg-1, i.p) was administered to induce amnesia and the memory was evaluated by using elevated plus-maze and passive avoidance tests. Piracetam (200 mg kg-1, i.p.) was used as a standard nootropic agent. The EO extract was administered intraperitoneally in four graded doses (150, 300, 450 and 600 mg kg-1) for 7 consecutive days to different groups of mice. The mice were sacrificed on the 8th day following assessment of memory. The brain malondialdehyde (MDA) and glutathione (GSH) as well as acetylcholinesterase (AchE)) activity was determined. It was observed that EO extract reversed the amnesia induced by scopolamine. The mean transfer latency and retention latency in the EO extract 600 mg kg-1 group vs the vehicle treated scopolamine group was 13.46 sec (p<0.001) and 134.4 sec (p<0.001) vs 23.99 sec and 44.55 sec, respectively. EO extract treatment also significantly (p<0.001) ameliorated the oxidative stress induced by scopolamine administration. The mice brain MDA and GSH levels in the EO extract 600 mg kg-1 group vs the scopolamine group were 29.95 nmol g-1 of wet tissue and 51.87 μg g-1 tissue vs 55.22 nmol g-1 of wet tissue and 28.33 μg g-1 tissue, respectively. Further, EO extract (300, 450 and 600 mg kg-1, i.p) significantly (p<0.001) reversed the rise in brain acetyl cholinesterase (AchE) level induced by scopolamine. The mice brain AchE levels in the EO extract 600 mg kg-1 group as compared to the scopolamine group was 70.23 vs 151.49 U mg-1 protein-1, respectively. These results suggest that EO possesses memory enhancing, antioxidant and anti-cholinesterase activity. It may be useful for the treatment of cognitive impairments induced by cholinergic dysfunction. Its potential in the management of dementia and Alzheimer disease needs to be further explored.