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目的:观察喜树碱对体外原代培养小鼠神经元的神经毒性作用。方法:利用原代培养的小鼠神经元,首先观察喜树碱对神经元活性影响的量效、时效关系。然后,将半数致死量的喜树碱作用于神经元后,通过TUNEL法、γ-H2AX免疫荧光标记、流式细胞法,检测神经元发生凋亡的情况。结果:喜树碱可明显抑制神经元的细胞活性,且呈浓度和时间依赖性。与对照组比较,喜树碱组神经元γ-H2AX和TUNEL阳性染色细胞明显增多;流式细胞仪检测,喜树碱组早期凋亡(27.8%)和晚期凋亡(4.7%)的发生率也显著增高。结论:喜树碱能抑制神经元活性,引起神经元DNA损伤,诱导神经元发生凋亡,其神经毒性的内在机制有待进一步研究。
OBJECTIVE: To observe the neurotoxicity of camptothecin on the primary cultured mouse neurons. Methods: Using primary cultured mouse neurons, first observe the effect of camptothecin on neuronal activity of the dose-effect, aging relationship. Then, after half the lethal dose of camptothecin was applied to neurons, neuronal apoptosis was detected by TUNEL method, γ-H2AX immunofluorescence labeling and flow cytometry. Results: Camptothecin significantly inhibited neuronal cell viability in a concentration and time-dependent manner. Compared with the control group, the expression of γ-H2AX and TUNEL positive neurons in the CPT group was significantly increased. The incidence of early apoptosis (4.7%) and camptothecin apoptosis in the CPT group Also significantly higher. CONCLUSION: Camptothecin can inhibit neuronal activity, cause DNA damage in neurons and induce neuronal apoptosis. The intrinsic mechanism of neurotoxicity remains to be further studied.