漆黄素逆转慢性应激鼠认知损害及其机制

Fisetin reverses cognitive impairment provoked by chronic stress and mechanism in mice

目的探讨漆黄素是否逆转慢性束缚应激小鼠认知损害及其机制。方法用CD1小鼠建立慢性束缚应激模型,漆黄素(25 mg·kg-1·d-1)灌胃给药14 d。Morris水迷宫检测空间学习记忆功能,Western blot检测相关蛋白表达变化。结果漆黄素明显改善应激鼠空间学习记忆功能,提高海马细胞外信号调节激酶ERK磷酸化水平,同时增加突触蛋白synapsin I、PSD95表达。ERK特异性阻断剂U0126完全阻断漆黄素改善认知。结论漆黄素改善慢性应激鼠认知功能,可能通过ERK通路调节神经可塑性有关。

Objective To investigate whether fisetin treatment prevents cognitive deficits provoked by chronic stress and mechanism in mice.Methods Mice were subjected to chronic restraint stress for 21 days.Stressed mice received repeated gavage of 25 mg·kg -1 fi-setin once daily for 14 consecutive days.Morris water maze （MWM）task was conducted for evaluating hippocampus -associated learning and memory.The expression levels of proteins in the hippocampus of mice were analyzed by western blot.Results Fisetin dramatically ameliorated the cognitive impairments in the stressed mice,rescued the decrease of hippocampal phospho -ERK level. Moreover,fisetin significantly improved synapse -associated proteins synapsin I and PSD95 expression.The ERK inhibitor,U0126, antagonize the fisetin -induced enhancement of cognitive function.Conclusions Fisetin improves cognitive deficits provoked by chron-ic stress in mice,which may attribute to ERK signaling pathway involved in the hippocampus.