摘要

Emerging evidence suggests that activated astrocytes play important roles in AD, and beta-asarone, a major component of Acorus tatarinowii Schott, was shown to be a potential therapeutic candidate for AD. While our previous study found that beta-asarone could improve the cognitive function of rats hippocampally injected with A beta, the effects of beta-asarone on astrocytes remain unclear, and this study aimed to investigate these effects. A rat model of A beta 1-42 (10 mu g) was established, and the rats were intragastrically treated with beta-asarone at doses of 10, 20, and 30 mg/kg or donepezil at a dose of 0.75 mg/kg. The sham and model groups were intragastrically injected with an equal volume of saline. Animals were sacrificed on the 28th day after administration of the drugs. In addition, a cellular model of A beta 1-42 (1.1 mu M, 6h) was established, and cells were treated with beta-asarone at doses of 0, 2.06, 6.17, 18.5, 55.6, and 166.7 mu g/mL. beta-Asarone improved cognitive impairment, alleviated A beta deposition and hippocampal damage, and inhibited GFAP, AQP4, IL-1 beta, and TNF-alpha expression. These results suggested that beta-asarone could alleviate the symptoms of AD by protecting astrocytes, possibly by inhibiting TNF-alpha and IL-1 beta secretion and then downregulating AQP4 expression.