Effect of ß-asarone in normal and ß-amyloid-induced Alzheimeric rats.

INTRODUCTION: ß-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 ß-asarone on neurodegeneration induced by intrahippocampal administration of ß-amyloid was investigated in adult male Wistar rats. MATERIAL AND METHODS: The rats were randomly divided into 9 groups: normal control, sham-operated control, ß-asarone (12.5, 25, and 50 mg/kg intragastrically, daily) alone, Alzheimeric control rats (ß-amyloid, intrahippocampal), ß-asarone (12.5, 25, and 50 mg/kg intragastrically, daily) together with ß-amyloid, and treatment was performed accordingly. Animals were injected with ß-amyloid bilaterally. Animals received ß-asarone daily using an intragastric tube for 50 days, starting from 30 days before administration of the ß-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 ß-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 ß-asarone decreased cell loss in the cerebral cortex and hippocampus in Alzheimeric rats. CONCLUSIONS: These results indicate that ß-asarone is effective in providing protection against oxidative stress and neuronal damage induced by ß-amyloid.

Maternal infection during late pregnancy increases anxiety- and depression-like behaviors with increasing age in male offspring.

Scientific reports suggest that the exposure to long-term stressors throughout or during late gestation increase anxiety- and depression-like behaviors of offspring in their later life. Moreover, several studies concluded that increasing age correlates with increased anxiety behaviors in humans and rodents. In the present study, we assessed the effects of prenatally administration of equal lipopolysaccharide (LPS) doses in various points of late gestation (days 15, 16, and 17) period, on neuroendocrine and immunological responses of pregnant mice, and subsequent long-lasting consequences of anxiety and depression with increasing age in male offspring at postnatal days (PD) 40 and 80. Four hours after the LPS injection, levels of corticosterone (COR) and pro-inflammatory cytokines (PIC) in pregnant mice, as compared to the control dams, were increased significantly. Furthermore, maternal inflammation raised the levels of COR, anxiety- and depression-like behaviors with increasing age in male offspring in comparison with saline male offspring. These data support other studies demonstrating that maternal stress increases the levels of anxiety and depression in offspring. Additionally, our data confirm other findings indicating that increasing age correlates with increased anxiety or depression behaviors in humans and rodents. Findings of this study suggest that time course of an inflammation response or stressor application during various stages of gestation and ages of offspring are important factors for assessing neuropsychiatric disorders.