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Effects of zibu piyin recipe(滋补脾阴方药) on SNK-SPAR Pathway in Neuron Injury Induced by Glutamate

Chinese Journal of Integrative Medicine 2008年第2期14卷 117-122页

作者：战丽彬隋华路小光孙长凯张建马辉 The Second Affiliated Hospital Dalian Medical University Department of Pathophysiology Dalian Medical University Department of Emergency Medicine Zhongshan Hospital Dalian University Department of Physiology Institute for Brain Disorder Dalian Medical University

Objective： To investigate the relationship between the excitotoxicity and seruminducible kinase （SNK） and spine-associated Rap GTPase-activating protein （SPAR） pathway in primary hippocampal neuron injury induced by glutamate and furthermore, to explore the molecular mechanism of neuroprotection of zibu piyin recipe （滋补脾阴方药, ZBPYR） and the relationship between ZBPYR and the morphological regulation of dendritic spines. Methods： The serum containing ZBPYR was prepared by seropharmacology. Reverse transcription and polymerase chain reaction （RT-PCR） was used to detect the expression of mRNA for SNK, SPAR, postsynaptic density protein 95 （PSD-95） and N-methyI-D-aspartate （NMDA） receptor subunits （NR1, NR2A and NR2B） in primary rat hippocampal neuron cultures after pretreatment with 10 μmol/L glutamate and ZBPYR serum. Results： ZBPYR serum pretreatment resulted in a significant down-regulation of glutamate-induced SNK mRNA expression （P〈0.05）. Significant up-regulation was seen on the mRNA expression of SPAR and PSD-95 （P〈0.05）. All these changes were dose-dependent. The mRNA expression of NR1, NR2A and NR2B was down-regulated to different degrees （P〈0.05）. Conclusion： The mechanism of effect of ZBPYR on glutamate-induced excitotoxicity may be related to the regulation of SNK-SPAR signal pathway. ZBPYR may play a role in protecting and maintaining the normal morphology and structure of dendritic spines, which may be achieved by inhibiting the excessive activation of NMDA receptors.

关键词： Alzheimer's disease zibu piyin recipe serum-inducible kinase spine-associated Rap GTPase-activating protein excitotoxicity dendritic spine

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