Xiang Xu1, Haibin Dai, Yulan Shi. 1. Department of Pharmacy, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Abstract
AIM: To investigate the neuroprotective effect of EPO against hypoxia, and determine the mechanism with respect to the EPO-induced neuroprotection. METHODS: Experiments were conducted using primary neuron cultures. Neuron survival and glutamate release were measured after bein insulted by hypoxia. Glutamate concentrations were determined by an HPLC-ECD system. RESULTS: Neurons were significantly damaged in hypoxia. Application of recombinant human EPO (10(-11) M) within 24 h before hypoxia significantly increased neuronal survival compared with no EPO treatment. Moreover, the enhancing of glutamate release stimulated by hypoxia was inhibited by pretreatment with EPO at a concentration of 10(-11) M. Further studies demonstrated that EPO also prevented glutamate and NMDA insulted neurotoxicity. CONCLUSION: These findings suggest that EPO prevents neuronal death in the cultured cortical neuron, possibly through attenuating both glutamate release and NMDA receptor evoked neurotoxicity pathway.
AIM: To investigate the neuroprotective effect of EPO against hypoxia, and determine the mechanism with respect to the EPO-induced neuroprotection. METHODS: Experiments were conducted using primary neuron cultures. Neuron survival and glutamate release were measured after bein insulted by hypoxia. Glutamate concentrations were determined by an HPLC-ECD system. RESULTS: Neurons were significantly damaged in hypoxia. Application of recombinant humanEPO (10(-11) M) within 24 h before hypoxia significantly increased neuronal survival compared with no EPO treatment. Moreover, the enhancing of glutamate release stimulated by hypoxia was inhibited by pretreatment with EPO at a concentration of 10(-11) M. Further studies demonstrated that EPO also prevented glutamate and NMDAinsulted neurotoxicity. CONCLUSION: These findings suggest that EPO prevents neuronal death in the cultured cortical neuron, possibly through attenuating both glutamate release and NMDA receptor evoked neurotoxicity pathway.