2010•Chinese Journal of Hospital PharmacyRequires access

Neuroprotective effect of tea polyphenol on mouse brain slices subjected to oxygen-glucose deprivation and glutamate injury

Lianjun Guo

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Abstract

OBJECTIVE To study the neuroprotective effect of tea polyphenol(TP)on mouse brain slices subjected to oxygen 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 MK801(0.03 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 neuroprotection against OGD/Glu-induced injury in mouse brain slices,which is probably partly through enhancing levels of SOD and through attenuating excitotoxicity mediated by NMDA receptor.

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OBJECTIVE To study the neuroprotective effect of tea polyphenol(TP)on mouse brain slices subjected to oxygen 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 MK801(0.03 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 neuroprotection against OGD/Glu-induced injury in mouse brain slices,which is probably partly through enhancing levels of SOD and through attenuating excitotoxicity mediated by NMDA receptor.

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Available abstract

OBJECTIVE To study the neuroprotective effect of tea polyphenol(TP)on mouse brain slices subjected to oxygen 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 MK801(0.03 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 neuroprotection against OGD/Glu-induced injury in mouse brain slices,which is probably partly through enhancing levels of SOD and through attenuating excitotoxicity mediated by NMDA receptor.

Key concepts: Neuroprotection, Glutamate receptor, Excitotoxicity, Pharmacology, Chemistry, NMDA receptor, Superoxide dismutase, Biochemistry

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