中文摘要：

目的：研究茶多酚（TP）对小鼠离体脑片氧糖剥夺（OGD）损伤及谷氨酸（Glu）损伤的神经保护作用。方法：建立恼片的OGD损伤及Glu损伤模型。TTC染色法和检测脑片在孵育液中乳酸脱氢酶（LDH）释放量用于评价脑片神经损伤的程度。测定OGD损伤脑片超氧化物歧化酶（SOD）活力。含镁离子、无镁离子人工脑脊液（ACSF）被用于进一步研究Glu损伤，并将TP与MK801的作用进行了比较。结果：TP（1，3，10mg·L^-1）可显著降低由OGD及Glu引起的皮层、海马脑片损伤。它也能显著增加OGD脑片的SOD活力。另外，1，3mmol·L^-1的Glu可显著降低全脑脑片的活性，且用含镁离子ACSF孵育的脑片活性均高于无镁离子ACSF孵育的脑片活性。TP（10mg·L^-1）与MK801（0.03mmol·L^-1）对Glu损伤脑片发挥了相似的神经保护作用，且两药的保护率不受此两种ACSF的影响。结论：TP对OGD损伤及Glu损伤小鼠离体脑片具有明显的神经保护作用，其保护作用可能与提高脑片组织SOD活力有关，也可能与减弱由NMDA受体兴奋所引起的神经元兴奋性毒性损伤有关。

英文摘要：

OBJECTIVE To study the neuroprotective effect of tea polyphenol （TP） on mouse brain slices subjected to oxy gen glucose deprivation （OGD） and glutamate （Glu） injury. METHODS The models of OGD and Glu injury in mouse brain slices were established. Neuronal damage was assessed by using TTC staining method and measurement of LDH release. Besides, SOD activity in OGD slices was assessed. And magnesium-contained/free ACSF was used to further study Glu injury, and the effects of TP and MK801 on Glu-injury slices were compared as well. RESULTS TP （1, 3,10 mg·L^-1） was able to prevent OGD/Glu-induced injury significantly in mouse cortical and hippocampal slices. It could also increase SOD activity in OGD slices greatly. In addition, 1,3 mmol·L^-1 of Glu markedly decreased the viability of the whole brain slices, and the viability of slices incubated with magnesium contained ACSF was constantly better than that relevantly incubated with magnesium free ACSF. TP （10 mg·L^-1 ） and MK8111 （ll. 03 mmol·L^-1） produced similar significant effects on Glu injury slices, and the protective rates of both the drugs were affected little by the two types ACSF. CONCLUSION TP can exert significant neuro protection against （K;D/Glu induced injury in mouse brain slices, which is probably partly through enhancing levels of SOD and through attenuating excitotoxieity mediated by NMDA receptor.