IL-33与TNF-α的协同作用对角质形成细胞增殖和凋亡的影响  

Synergistic Effect of IL-33 and TNF-α on the Proliferation and Apoptosis of Keratinocytes

作　　者：付丹丹[1] 胡华[1] 李占国[1] 李敏[1] 田中伟[1] 

机构地区：[1]新乡医学院第一附属医院皮肤性病科,河南卫辉453100

出　　处：《中国皮肤性病学杂志》2016年第7期683-686,690,共5页The Chinese Journal of Dermatovenereology

基　　金：河南省医学科技攻关计划重点项目(201502016);河南省教育厅科学技术研究重点项目(13A320852);河南省中青年卫生科技创新人才工程专用基金(201004159)

摘　　要：目的研究白细胞介素33(IL-33)和肿瘤坏死因子α(TNF-α)的协同作用对角质形成细胞增殖和凋亡的影响及其调节机制。方法分别构建腺病毒表达载体AAV-IL-33和AAV-TNF-α转染HaC aT细胞。将细胞随机分为4组:control组,IL-33组,TNF-α组和L-33+TNF-α组。Western blot法检测各组细胞中IL-33和TNF-α的水平,MTT法检测细胞增殖,流式细胞术检测细胞凋亡水平,ELISA检测IL-6,IL-8和IFN-γ的含量,并检测细胞核内NF-κB和IκBα蛋白的磷酸化水平。结果 IL-33和TNF-α能够促进HaC aT的增殖并降低其凋亡,提升IL-6,IL-8和IFN-γ的含量,增加细胞中NF-κB和IκBα的蛋白水平,且在其协同作用下效果更加显著。结论 IL-33和TNF-α的协同作用能增强HaC aT细胞增殖和炎症反应水平,抑制细胞凋亡,这可能与NF-κB信号通路的激活有关。Objective To investigate the synergistic effect of interleukin-33 （IL-33） and tumor necrosis factor α （TNF- α） on keratinocyte proliferation and apoptosis and the underlying mechanism. Methods Adeno-associated virus （AAV）-IL-33 and AAV-TNF-α were constructed and transfected into HaCaT cells separately. The protein expression levels of IL-33 and TNF-α were detected by western blot. Cell proliferation was measured by MTY. Cell apoptosis was detected by flow cytometry. The concentrations of IL-6, IL-8 and IFN-γ were detected by ELISA, and the protein phosphorylation level of NF-κB and IκBα were measured. Results IL- 33 and TNF-α overexpression elevated cell proliferation, inhibited cell apoptosis, promoted the concentrations of IL-6, IL-8 and IFN-γ, increased the expression of NF-KB and IκBα. Additionally, the effects were more significant with synergistic transfection of IL-33 and TNF-α. Conclusion The synergistic effect of IL-33 and TNF-α elevated the proliferation and inflammation, and inhibited apoptosis of HaCaT cells through activation of NF-KB signaling pathway.

关 键 词：角质形成细胞 白介素-33 肿瘤坏死因子-Α 核因子-ΚB 

分 类 号：R751[医药卫生—皮肤病学与性病学]