Effect of β-asarone in normal and β-amyloid-induced Alzheimeric rats

INTRODUCTION: β-Asarone is a major component of Acorus tatarinowii Schott. It has pharmacological effects that include antihyperlipidemic, anti-inflammatory, and antioxidant activity. In the present study, the effect of β-asarone on neurodegeneration induced by intrahippocampal administration of β-amyloid was investigated in adult male Wistar rats. MATERIAL AND METHODS: The rats were randomly divided into 9 groups: normal control, sham-operated control, β-asarone (12.5, 25, and 50 mg/kg intragastrically, daily) alone, Alzheimeric control rats (β-amyloid, intrahippocampal), β-asarone (12.5, 25, and 50 mg/kg intragastrically, daily) together with β-amyloid, and treatment was performed accordingly. Animals were injected with β-amyloid bilaterally. Animals received β-asarone daily using an intragastric tube for 50 days, starting from 30 days before administration of the β-amyloid. The rats were sacrificed and parameters of oxidative stress, superoxide dismutase (SOD) and glutathione peroxidase (GPX) activity were measured in hippocampus homogenate. Histopathological changes were examined by Bielschowsky staining. RESULTS: Our results showed that administration of β-asarone (25 and 50 mg/kg) significantly increased the levels of antioxidant enzymes, including SOD (1.09 ±0.02, 1.21 ±0.02, p < 0.001, respectively) and GPX (58.94 ±0.78, 68.92 ±3.64, p < 0.001, respectively) in comparison with Alzheimeric control rats (SOD and GPX level for Alzheimeric control group: 0.44 ±0.01, 35.09 ±1.15, respectively). Histopathological examination showed that β-asarone decreased cell loss in the cerebral cortex and hippocampus in Alzheimeric rats. CONCLUSIONS: These results indicate that β-asarone is effective in providing protection against oxidative stress and neuronal damage induced by β-amyloid.