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目的:探讨PrP10 6- 12 6对神经元的毒性作用。方法:原代培养的皮质神经元暴露于合成多肽PrP10 6 -12 6,观察细胞存活率的变化,采用流式细胞术检测有无凋亡的发生,用免疫印迹法检测caspase 3的活性。结果:在PrP10 6 -12 6的作用下,神经元存活数较对照组减少,随着作用时间的延长,存活率明显下降。在PrP10 6- 12 6作用下神经元的凋亡比例明显增加,PrP10 6- 12 6组凋亡细胞为2 4.93 % ,对照组为6.95 %。与对照组比,PrP10 6 -12 6组在培养第6、8、10天时均有较明显的caspase- 3表达,且伴有caspase 3的活化。结论:PrP10 6- 12 6对原代培养的皮质神经元有毒性作用,呈时间依赖性。PrP10 6 -12 6毒性作用涉及了细胞凋亡机制,激活caspase -3诱导细胞凋亡可能是途径之一。
Objective: To investigate the toxic effect of PrP10 6- 12 6 on neurons. Methods: Primarily cultured cortical neurons were exposed to the synthetic peptide PrP10 6 -12 6 to observe the changes of cell viability. The apoptosis was detected by flow cytometry. The activity of caspase 3 was detected by Western blotting. Results: PrP10 6 -12 6 under the action of neuronal survival than the control group decreased, with the extension of time, the survival rate decreased significantly. The percentage of apoptotic neurons in PrP10 6- 12 6 cells was significantly increased, while that of PrP10 6- 12 6 cells was 2.93% and that of the control group was 6.95%. Compared with the control group, PrP10 6 -12 6 group had obvious caspase-3 expression on the 6th, 8th and 10th day after culture, accompanied by the activation of caspase-3. Conclusion: PrP10 6- 12 6 has a toxic effect on primary cultured cortical neurons in a time-dependent manner. PrP10 6 -12 6 toxicity is involved in the mechanism of apoptosis, activation of caspase -3-induced apoptosis may be one of the ways.