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作 者:孙敏[1] 张磊[2] 宋淑玲[3] 陈作雷[4] 刘英志[4] 殷积慧[4]
机构地区:[1]青岛大学医学院,山东青岛266071 [2]上海交通大学医学院附属第九人民医院,上海200011 [3]滨州市中心医院,山东滨州251700 [4]青岛大学附属医院,山东青岛266000
出 处:《现代生物医学进展》2015年第15期2840-2844,共5页Progress in Modern Biomedicine
基 金:The National Natural Science Foundation of China(81300934)~~
摘 要:目的:探讨七氟烷对培养的小鼠小胶质细胞中炎症因子表达的影响。方法:取新生(2~3天)C57BL/6小鼠,分离小胶质细胞,将其随机分为4组(n=10):对照组(Control);七氟烷组(Sevoflurane);NF-κB抑制剂组(PDTC);NF-κB抑制剂+七氟烷组(PDTC+Sevoflurane)。用Drager麻醉机向Sevoflurane组PDTC+Sevoflurane组培养的小胶质细胞盒内释放21%O2,5%CO2,4.1%七氟烷的气体,用气体分析仪持续监测各组的浓度。应用Iba-1的免疫荧光染色法对小鼠小胶质细胞进行纯度鉴定。分别在于给七氟烷后2 h、4 h和6 h时采用免疫印迹分析技术检测两组小胶质细胞IL-6和TNF-α的表达水平和NF-κB的活性。PDTC+Sevoflurane组在给七氟烷前一小时给予PDTC,采用ELISA技术和免疫印迹分析技术检测各组小胶质细胞IL-6和TNF-α的浓度和NF-κB的表达。结果:免疫印迹显示七氟烷组细胞中IL-6、TNF-α水平和NF-κB的激活水平升高;PDTC降低了七氟烷作用后核内NF-κB的表达,减弱了IL-6和TNF-α水平的升高作用。结论:七氟烷可通过激活NF-κB信号通路,进一步激活培养的小鼠小胶质细胞中炎症因子的表达。Objective: To evaluate effect of sevoflurane on the expression of inflammation cytokine in neuroglioma cells of cul- tured mice. Methods: Microglia cells abtained fiom newborn (2-3 days) C57BL/6 mice were separated and randomly divided into 4 groups (n=10): control group (Control); sevoflurane group (Sevoflurane); NF-KB inhibitors group (PDTC); NF-KB inhibitors group+ sevoflurane group (PDTC+Sevoflurane). Oxygen (21%), Carbon dioxide (5 %) and sevoflurane(4.1%) were delivered from an Drager anesthesia machine to the microglia cells sealed in a plastic box of the two groups. The two groups are Sevoflumne group and PDTC+Sevoflumne group in which the later group had been given PDTC 1 hour before sevoflurane treatment. A Drag gas analyzer was used to continuously monitor the concentrations of the 02, CO2 and sevoflurane respectively. Iba-1 immunofluorescence staining method was used to the purity identification of microglia in mice. We examined the expression of IL-6 and TNF-a (by Western Blotting Analysis and ELISA)and activation of NF-KB (by Western Blotting Analysis) at 2,4 and 6h after sevoflurane treatment. Results: Sevoflurane increases levels of IL-6 and TNF-a through activates NF-kB signaling pathway. Conclusion: These studies suggest that NF-kB signaling pathway could contribute to the increasing expression of inflammation cytokine.
关 键 词:七氟烷 神经炎症 IL-6 TNF-α NF-ΚB
分 类 号:R164.1[医药卫生—公共卫生与预防医学]
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