N-花生四烯甘氨酸（NAGly）缓解七氟烷诱导的发育期大鼠原代海马神经元神经毒性

目的探讨N-花生四烯酰乙醇胺（N—arachidonoylethanolamine，AEA）类似物N-花生四烯甘氨酸（N—arachidonoylglycine，NAGly）对发育期大鼠原代海马神经元七氟烷暴露诱导的神经毒性的保护作用。方法体外培养7d的原代海马神经元经七氟烷暴露，同时给予NAGly处理，采用TUNEL染色和流式检测细胞凋亡。Westernblot检测凋亡蛋白表达。结果NAGly促进细胞活性，抑制了七氟烷诱导的凋亡。NAGly改善了七氟烷暴露诱导的ERKI／2活性抑制。MEK抑制剂能够破坏NAGly的神经保护作用。结论AEA类似物NAGly能够保护发育期海马神经元改善七氟烷诱导的神经毒性，其可能机制是通过上调MEK／ERKl／2MAPK信号通路实现的。

NAGIy ameliorated Sevoflurane induced neurotoxicity in developing rat primary hippocampal neurons

Objective To determine the neuroprotective effect of N - arachidonoyl glycine （NAGly） on developmental Sevoflurane（Sev） neurotoxicity in rat primary hippocampal neurons. Methods DIV 7 primary hippocampal neurons were treated with Sev or Sev along with NAGly. TUNEL and flow cytometry were used to detect the apoptosis and cell viability. Western blot was used to measure the protein levels of apoptosis pathway molecules. Results NsTyr promoted cell viability and suppressed apoptosis in Sev neurotoxicity. NAGly rescued Sev induced inhibition of ERK1/2. Inhibition of MEK dis- rupted the protective effect of NAGly on Sev neurotoxieity. Conclusion AEA analog NAGly protects the developing hippocampal neurons against Sev neurotoxicity partially by MEK/ERK1/2 MAPK signaling pathway.