Aim To investigate the effects of 17β-es-tradiol on the apoptosis induced by ketamine in primary cultured cortical neurons. Methods Primary cultured cortical neurons were treated with different concentra-tions of ketamine or 17β-estradiol respectively. 24 hours after various treatments, neuron viability was measured by MTT assay. The structure of neurons was analyzed using microscope. Apoptotic neurons were de-termined by the TUNEL assay. The level of pAkt ex-pression was analyzed by Western blot. ResultsCompared with the control group, ketamine decreased neuron viability in a dose-dependent manner. Com-pared with ketamine group, 17β-estradiol increased neuron viability in a dose-dependent manner. Lack of three-dimensional sense,faded color,uncleared outline were observed, and fractured neuron axons or neurons death were also observed in neurons treated by 100μmol · L-1 ketamine. 100 μmol · L-1 ketamine in-creased the number of apoptotic neurons and decreased the expression of pAkt. 0.1 μmol · L-1 17β-estradiol decreased the number of apoptotic neurons and in-creased the expression of pAkt. LY294002 inhibited the protective effects of 17β-estradiol, the number of apoptotic neurons increased, and the level of pAkt de-creased significantly. Conclusion 17β-estradiol ex-erts the neuroprotective effects against ketamine-in-duced neuroapoptosis by activating the PI3 K/Akt sig-naling pathway.%目的：研究17β雌二醇对氯胺酮诱导的原代培养皮层神经元凋亡的影响。方法原代培养大鼠皮层神经元,分别给予不同浓度的氯胺酮及17β雌二醇培养24 h,MTT法检测神经元的存活率,显微镜下观察神经元的形态变化, TUNEL法检测神经元调亡,Western blot法测定pAkt蛋白的表达。结果与对照组比较,氯胺酮能剂量依赖性降低神经元存活率。与氯胺酮组比较,17β雌二醇能剂量依赖性提高神经元的存活率。100μmol·L-1氯胺酮组显微镜下神经元数量减少,胞体立体感消失,细胞轮廓不清,神经元轴突断裂,TUNEL阳性神经元明显增加, pAkt表达明显降低。0.1
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