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

发布时间：2018-11-23 10:06

【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。
[Abstract]:Objective to study the synergistic effect of interleukin 33 (IL-33) and tumor necrosis factor 伪 (TNF- 伪) on the proliferation and apoptosis of keratinocytes and its regulatory mechanism. Methods Adenoviral expression vectors AAV-IL-33 and AAV-TNF- 伪 were constructed and transfected into HaC aT cells. The cells were randomly divided into four groups: control group, IL-33 group, TNF- 伪 group and L-33 TNF- 伪 group. The levels of IL-33 and TNF- 伪 were detected by. Western blot assay, the proliferation of cells were detected by MTT assay, and apoptosis was detected by flow cytometry. ELISA was used to detect the contents of IL-6,IL-8 and IFN- 纬, and the phosphorylation levels of NF- 魏 B and I 魏 B 伪 proteins in the nucleus. Results IL-33 and TNF- 伪 could promote the proliferation and decrease the apoptosis of HaC aT, increase the content of IL-6,IL-8 and IFN- 纬, and increase the protein levels of NF- 魏 B and I 魏 B 伪. Conclusion the synergistic effect of IL-33 and TNF- 伪 can enhance the proliferation and inflammatory response of HaC aT cells and inhibit apoptosis, which may be related to the activation of NF- 魏 B signaling pathway.
【作者单位】：新乡医学院第一附属医院皮肤性病科;
【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)
【分类号】：R758.63

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