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目的探讨GCN5活性对神经元存活和凋亡的作用。方法体外培养小脑颗粒神经元,用GCN5抑制剂CPTH2和MB3处理神经元24 h后,核染色检测神经元的凋亡率,Western blot检测H3K9的乙酰化及Caspase 3活性。结果 CPTH2和MB3浓度依赖抑制了H3K9乙酰化,CPTH2和MB3浓度和时间依赖地诱导了神经元凋亡(P<0.05),且激活了Caspase 3。结论 GCN5活性对神经元存活起关键作用。
Objective To investigate the effect of GCN5 activity on neuronal survival and apoptosis. Methods Cerebellar granule neurons were cultured in vitro. Neurons were treated with GCN5 inhibitor CPTH2 and MB3 for 24 h. The apoptosis rate of neurons was detected by nuclear staining. The acetylation and Caspase 3 activity of H3K9 were detected by Western blot. Results CPTH2 and MB3 inhibited the acetylation of H3K9 in a dose - dependent manner. CPTH2 and MB3 induced neuronal apoptosis in a dose - and time - dependent manner (P <0.05) and activated Caspase 3. Conclusion GCN5 activity plays a key role in the survival of neurons.