【摘要】 目的研究丙泊酚对氧糖剥夺(OGD)导致神经元样鼠嗜铬细胞瘤(PC12)细胞损伤的影响及机制。方法用神经生长因子(7S-NGF)将PC12细胞分化为神经元样PC12细胞,于37℃、5%CO2+95%N2中孵育1、6、12、24和48h后,用MTT法获得细胞损伤最明显的时间;用1、5、10μmol/L的丙泊酚分别处理OGD损伤的细胞,通过MTT法得出对细胞作用最显著的浓度。细胞分为3组:正常对照组、OGD组和OGD+丙泊酚组,用免疫细胞化学染色和Western blot评估丙泊酚的作用及机制。结果 PC12细胞OGD损伤12h后,观察到约70%的细胞损伤;10μmol/L丙泊酚处理细胞后,细胞活力增加最为显著(P<0.01);OGD+丙泊酚组磷酸化应激活化蛋白激酶(SAPK)/Jun氨基末端激酶(JNK)和c-Jun的表达明显低于OGD组(P<0.05)。结论丙泊酚通过SAPK/JNK-c-Jun信号通路保护OGD损伤的PC12细胞。更多还原

【Abstract】 Objective To investigate the effect and mechanism of propofol on oxygen-glucose deprivation(OGD)caused rat pheochromocytoma cells(PC12)injury.Methods PC12 cells were differentiated into neuron-like PC12 cells by nerve growth factor(7 S-NGF)and then incubated in 5% CO2+95% N2 for 1,6,12,24 and 48 h.MTT method was used to detect the most obvious time of cell injury.OGD-injured PC12 cells were treated with 1μmol/L,5μmol/L and 10μmol/L propofol respectively,and the propofol concentration which had most significant effect on cells was obtained by using the MTT method.The cells were randomly divided into three groups:normal control group,OGD group and OGD+propofol group.The effect and mechanism of propofol were evaluated by immunocytochemical staining and Western blot.Results After PC12 cells OGD injury for 12 h,the injury of about 70%cells was observed;after 10μmol/L propofol treating the cells,the cellular viability increase was most significantly(P<0.01).The expression of phosphorylated SAPK/JNK and c-Jun in the OGD+ propofol group was significantly lower than that in the OGD group(P<0.05).Conclusion Propofol protects OGD injured PC12 cell through SAPK/JNK-c-Jun signal pathway.更多还原