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The present study was designed to investigate the neuroprotective effect of Hibiscus rosa sinensis L. in aluminuminduced neurotoxicity in rats. The animals were treated with aluminium chloride (4.2 mg/kg, p.o) for 21 days to induce oxidative stress. The methanolic extract of Hibiscus rosa sinensis (HRS - 100, 200 and 300 mg/kg/day, p.o, for 21 days) was administered 30 min before aluminum. The elevated plus-maze paradigm was used to assess the effect of HRS on aluminum-induced memory impairment. Animals were sacrificed on 21st day, brains were isolated and biochemical estimations were performed. The aluminium treated group showed significant increase in transfer latency (TL) on day 20th and 21st indicating impairment of memory. Administration of HRS (100 - 300 mg /kg, p.o) significantly (p < 0.01) reversed the memory impairment. Biochemical analysis of brain revealed that the chronic administration of aluminium significantly increased lipid peroxidation and decreased levels of catalase (CAT) and glutathione reductase (GSH), an index of oxidative stress process. Administration of extract significantly (p < 0.01) attenuated the lipid peroxidation; and reversed the decrease in brain CAT and GSH levels (p < 0.01). The superoxide dismutase (SOD) levels were increased after aluminium treatment which was normalized by HRS (p < 0.01). The results strengthen the oxidative stress hypothesis of aluminium- induced neurotoxicity and suggest the beneficial role of HRS in the management of Alzheimer's disease and oxidative stress. Cognitive-enhancing activity of HRS may be exerted through antioxidant mechanism.


Hibiscus rosa sinensis, Aluminium, Elevated Plus-maze, Lipid Peroxidation, Oxidative Stress
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