中文摘要：

目的 探究咖啡酸苯乙酯对脂多糖诱导的小胶质细胞BV-2神经炎症反应的抑制作用及其潜在的作用机制。方法 采用脂多糖（1μg·mL-1）诱导小胶质细胞BV-2活化,制作炎症反应模型,利用四甲基偶氮唑蓝法检测细胞存活率,并用酶联免疫法测定咖啡酸苯乙酯对炎症因子一氧化氮、白细胞介素-1β和白细胞介素-6合成释放的影响。然后用蛋白印迹法研究了咖啡酸苯乙酯对炎症相关蛋白（诱导型一氧化氮合酶、环氧化酶-2、IκB以及P-IκB）表达的作用。此外,进一步研究了咖啡酸苯乙酯对炎症转录因子NF-κB核转位的作用。结果 咖啡酸苯乙酯与脂多糖（1μg·mL^-1）同时作用于BV-2小胶质细胞,分别于温箱中孵育24、8 h收集上清液,检测一氧化氮、白细胞介素-1β、白细胞介素-6的释放量。结果显示,脂多糖（1μg·mL^-1）可以造成细胞损伤,增加炎症因子释放,咖啡酸苯乙酯则可以降低脂多糖诱导的小胶质细胞对一氧化氮、白细胞介素-1β和白细胞介素-6的释放,并可抑制诱导型一氧化氮合酶、环氧化酶-2、P-IκB、P-NF-κB蛋白的表达,还可以抑制NF-κB的核转位。结论 上述研究说明,咖啡酸苯乙酯（5,10,20μmol·L-1）可以通过抑制炎性因子的表达而减少对小胶质细胞的损伤,其抗炎活性可能是通过抑制NF-κB信号通路介导的炎症反应实现的。

英文摘要：

OBJECTIVE To investigate the inhibitory effects of caffeic acid phenethyl ester （CAPE） on LPS-induced inflammatory responses in BV-2 microglial cells and its mechanism. METHODS The model was build by BV-2 microglial cells induced by LPS （μg·mL^-1 ） , which was used to inspect the cell survivability by means of MTT, investigate the effect of CAPE on the release of inflammatory factor NO, IL-1β, IL-6 by ELISA, and the expression of inflammation-related protein （iNOS, COX-2, IκB, P-IKB, NF- κB, P-NF-κB） were analyzed by used of Western Blot. Finally, the regulatory effects of CAPE on inflammatory transcription factor NF- κB activation were inspected. RESULTS CAPE and LPS affected on BV-2 cells, which are collected after being incubated at 37 for 24 or 8 h, then test the release of NO, IL-1 β, IL-6. As is shown, LPS （ 1 μg·mL^-1 ） can injury the cells,and increase inflammatory cytokines. CAPE （5, 10, 20 μg·mL^-1 ） can decrease these inflammatory cytokines, down-regulate iNOS, COX-2, IKB, P-IKB expression and restrain NF-κB nuclear transloeation. CONCLUSION The anti-inflammatory activity of CAPE may be achieved through inhibiting NF-κB signaling pathway.