目的：探讨漆黄素逆转慢性束缚应激小鼠认知损害的突触可塑性研究。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，漆黄素给药前30 min 双侧背侧海马微量注射 U0126（0．5μg／侧）。场电生理研究海马CA1区长时程增强（LTP）的变化，高尔基染色观察树突棘数量改变，Western blot 检测突触膜蛋白表达。结果漆黄素逆转慢性应激鼠海马 CA1区 LTP 损害，提高海马树突棘数量，ERK 特异性阻断剂 U0126阻断其效应。结论漆黄素逆转慢性应激鼠海马突触可塑性损害，可能与 ERK 通路有关。%Objective To investigate synaptic plasticity following the prevention of cognitive deficits by fisetin treatment provoked by chronic stress in mice.Methods Mice were subjected to chronic restraint stress for 21 days.Stressed mice received repeated gavage of 25 mg·kg -1 fisetin once daily for 14 consecutive days.Mice were injected with U0126(0.5 μg/side)30 min before fisetin treatment. Effects of fisetin on long-term potentiation (LTP)in mouse hippocampal slices were investigated by electrophysiological methods.The expressive levels of proteins in the hippocampus of mice were analyzed by Western blot.The spine density in mice was investigated by Golgi staining.Results Fisetin reversed hippocampal LTP in stressed mice,increased the density of dendritic spines.However,pre-treatment with U0126,a specific ERK inhibitor,blocked the restoration of synaptic plasticity by fisetin in stressed mice.Conclusions Chronic oral administration of fisetin restores synaptic plasticity in stressed mice,which may be related to ERK signaling pathway in-volved in the hippocampus.
展开▼
