Effect of paeonol on EAA,NMDA receptor in cultured rat hippocampal neurons subjected to oxygen-glucose deprivation / reperfusion-induced injury

Objective To observe the effect of paeonol on excitatory amino acid( EAA),N-methyl-D-aspartate( NMDA) receptor expression in cultured rat hippocampal neurons subjected to oxygen-glucose deprivation / reperfusion( OGD/ R)-induced injury and to investigate its neuroprotective mechanism. Methods We divided rat hippocampal neurons which were primarily cultured for 8-12 d into four groups: the control group,OGD/ R group,paeonol treatment group and MK-801 group,and then we established the models of OGD/ R-induced injury,paeonol and MK-801 solution were separately injected into rats of the paeonol treatment group and MK-801 group at each reperfusion time points. The morphological changes of neurons were observed by the inverted phase-contrast microscopy,the neuron viability was measured by MTT assay,the binding force of NMDA receptor was valuated by liquid scintillation counting,the expression of NMDA receptor NR1 subunit mRNA was detected by RT-PCR,and the content of EAA was detected by amino acid analyzer. Results Neurons in the OGD/ R group were swollen or deformed,with short processes and then gradually disappeared; the granules of cytoplasm were significantly degenerative,and even completely disintegrated. The morphological changes of neurons in paeonol group and MK-801 group were reduced as compared with the OGD/ R group,and with integrated cell body,clear neurite; compared with the control group,the neuron survival rate was significantly decreased,binding capacity,NMDA receptor NR1 subunit mRNA expression and EAA content were significantly increased in the OGD/ R group. Indexes were significantly improved in the paeonol group and MK-801 group as compared with that in OGD/ R group( all P 0. 05). Conclusion The paeonol has the protective effect on rat neurons subjected to OGD/ R-induced injury,whose mechanism may be associated with the inhibition of EAA and NMDA receptor expression.