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作 者:刘亚坤[1] 纪乐 于利双 李忠尧[1] 李春岩[1] 李媛媛[1] Liu Yakun;Ji Le;Yu Lishuang;Li Zhongyao;Li Chunyan;Li Yuanyuan(Department of Neurology,the Second Hospital of Hebei Medical University,Shijiazhuang 050000,China)
机构地区:[1]河北医科大学第二医院神经内科,石家庄050000 [2]河北医科大学第一医院神经外科
出 处:《脑与神经疾病杂志》2023年第3期147-150,共4页Journal of Brain and Nervous Diseases
基 金:国家自然科学基金资助项目(81901290)。
摘 要:目的观察干扰素调节因子5(interferon-regulatory factor 5,Irf5)对肌萎缩侧索硬化(amyotrophic lateral sclerosis,ALS),TDP-25细胞模型的影响。方法利用慢病毒感染的方法,建立过表达Irf5的TDP-25稳转细胞株,在基因及蛋白水平鉴定其表达效率,倒置显微镜下观察细胞的形态学变化,通过实时荧光定量PCR方法比较过表达Irf5后对TDP-25细胞的影响,包括细胞凋亡、细胞周期以及炎症因子的产生。结果过表达Irf5后,与细胞凋亡有关的指标Caspase-3、Caspase-8和Bak1都较对照组有所增加。细胞周期调控蛋白,P21的表达增加。炎症因子包括肿瘤坏死因子(tumor necrosis factorα,TNF-α)、白细胞介素-6(interleukin-6,IL-6)、白细胞介素-12p40(IL-12p40)的表达都有所增加,与对照组相比,差异有统计学意义。结论Irf5促进TDP-25细胞的凋亡、细胞周期阻滞,以及产生促炎细胞因子,加速了细胞的死亡。Objective To observe the effect of interferon regulatory factor 5(Irf5)on the TDP-25 cell model of amyotrophic lateral sclerosis(ALS).Methods Using lentivirus infection method,TDP-25 stably transfected cell line which was overexpressed Irf5 was established.The expression efficiency was identified at gene and protein levels.Morphological changes were observed under inverted microscope.The effects of overexpressing Irf5 on TDP-25 cells were compared by qPCR method,including apoptosis,cell cycle and the production of inflammatory factors.Results After overexpression of Irf5,the apoptosis related markers Caspase-3,Caspase-8 and Bak1 were increased compared with the control group.The expression of cell cycle regulatory protein,P21 was increased.The levels of inflammatory factors include TNF-αIL-6 and IL-12 were increased,and there were significant differences compared with the control group.Conclusion Irf5 promotes the apoptosis,cell cycle arrest,and the production of proinflammatory cytokines of TDP-25 cells,and accelerates cell death.
关 键 词:肌萎缩侧索硬化 干扰素调节因子5 细胞凋亡 炎症因子
分 类 号:R744.8[医药卫生—神经病学与精神病学]
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