Neuroprotective effect of ethanolic extract of Sida acuta in mercuric chloride-induced brain damage in rats.
Mercuric chloride has useful applications but exhibits toxicity which affects the central nervous system thus causing health hazards. Antioxidants reduce the oxidative damage associated with mercury intoxication. We tested the hypothesis that administration of antioxidant-containing ethanolic extract Sida acuta (EESA) should attenuate the effect of mercuric chloride (HgCl2) in brain of rat. Twenty male rats were randomized into four groups (n=5): Group A: Control, distilled water; Group B: EESA (200 mg/kg bwt); Group C: HgCl2 (4 mg/kg bwt); Group D: HgCl2 (4 mg/kg bwt) + EESA (200 mg/kg bwt). All treatments lasted seven days and were given orally by gavage. All rats were euthanized on day 8 of the experiment after conducting behavioural tests. Biochemical parameters namely: malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) and brain tissue were examined with regard to histotological and histomorphometric parameters. Mercuric chloride significantly (p<0.05) elevated the level of MDA and reduced the level of GSH, activities of SOD and CAT significantly (p<0.05) relative to control. It also neuronal degeneration and significantly (p<0.05) reduced the densities of viable of the cerebral cortex, dentate gyrus, pyramidal neurons of cornu ammonis of hippocampus, and Purkinje neurons of the cerebellum when compared with control. In Group D rats, the altered parameters were reversed to near control values significantly (p<0.05), histological alterations were improved relative to HgCl2-treated group. Data demonstrated that HgCl2 exposure induced a significant degeneration in the cerebral cortex, dentate gyrus, cornu ammonis and cerebellum of Wistar rats which concomitantly administration of EESA with HgCl2 ameliorated.
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