抑制聚二磷酸腺苷核糖聚合酶1减轻尼古丁诱导的人支气管上皮细胞炎症反应的研究
发布时间：2018-08-03 20:34
【摘要】：目的：通过检测尼古丁刺激的人支气管上皮细胞中炎症因子的变化,探讨了抑制聚二磷酸腺苷核糖聚合酶1(PARP1)在尼古丁诱导的Toll样受体4(TLR4)介导的人支气管上皮细胞炎症反应中的作用和机制。 材料与方法：培养人支气管上皮细胞。通过实时定量PCR、蛋白印迹、小干扰RNA的转染以及免疫荧光等方法,分别检测尼古丁刺激组及其阴性对照组、TLR4和PARP1抑制组及其阴性对照组中炎症因子相关基因、蛋白的表达量。 结果：与对照组相比较,尼古丁刺激增加了TLR4和PARP1的蛋白表达。TLR4抑制减少了尼古丁诱导的诱导型一氧化氮合酶(iNOS)、细胞间粘附分子1(ICAM-1)和PARP1的上调。核因子κB的抑制减少了iNOS和ICAM-1的表达。抑制PARP1通过阻止核因子κB的核转位而减少了尼古丁诱导的炎症因子表达。 结论：我们的研究显示尼古丁刺激支气管上皮细胞,通过TLR4/PARP1/NF-κB途径诱导ICAM-1和iNOS的表达。在尼古丁诱导、TLR4介导的炎症反应中,PARP-1或许是不可或缺的因素。在支气管上皮细胞炎症反应中,PARP-1抑制或许是治疗尼古丁诱导的炎症因子表达的有效手段。
[Abstract]:Objective: to detect the changes of inflammatory factors in human bronchial epithelial cells stimulated by nicotine. The role and mechanism of inhibition of adenosine diphosphate polymerase 1 (PARP1) in nicotine-induced Toll-like receptor 4 (TLR4)-mediated inflammation of human bronchial epithelial cells was investigated. Materials and methods: human bronchial epithelial cells were cultured. By real-time quantification of RNA, Western blot, transfection of small interfering RNA and immunofluorescence, the expression of inflammatory factor-related genes and proteins in the nicotine stimulated group and its negative control group were detected, respectively. Results: compared with the control group, nicotine stimulation increased the protein expression of TLR4 and PARP1. TLR4 inhibited the up-regulation of ICAM-1 and PARP1 induced by nicotine. The inhibition of NF- 魏 B reduced the expression of iNOS and ICAM-1. Inhibition of PARP1 reduces nicotine-induced inflammatory factor expression by blocking nuclear translocation of NF-魏 B. Conclusion: our study shows that nicotine stimulates bronchial epithelial cells and induces the expression of ICAM-1 and iNOS through TLR 4 / PARP 1 / NF- 魏 B pathway. PARP-1 may be an indispensable factor in nicotine-induced TLR 4-mediated inflammatory response. Inhibition of PARP-1 may be an effective method for the treatment of nicotine-induced inflammatory factor expression in bronchial epithelial cells.
【学位授予单位】：山东大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R363
本文编号：2162922
[Abstract]:Objective: to detect the changes of inflammatory factors in human bronchial epithelial cells stimulated by nicotine. The role and mechanism of inhibition of adenosine diphosphate polymerase 1 (PARP1) in nicotine-induced Toll-like receptor 4 (TLR4)-mediated inflammation of human bronchial epithelial cells was investigated. Materials and methods: human bronchial epithelial cells were cultured. By real-time quantification of RNA, Western blot, transfection of small interfering RNA and immunofluorescence, the expression of inflammatory factor-related genes and proteins in the nicotine stimulated group and its negative control group were detected, respectively. Results: compared with the control group, nicotine stimulation increased the protein expression of TLR4 and PARP1. TLR4 inhibited the up-regulation of ICAM-1 and PARP1 induced by nicotine. The inhibition of NF- 魏 B reduced the expression of iNOS and ICAM-1. Inhibition of PARP1 reduces nicotine-induced inflammatory factor expression by blocking nuclear translocation of NF-魏 B. Conclusion: our study shows that nicotine stimulates bronchial epithelial cells and induces the expression of ICAM-1 and iNOS through TLR 4 / PARP 1 / NF- 魏 B pathway. PARP-1 may be an indispensable factor in nicotine-induced TLR 4-mediated inflammatory response. Inhibition of PARP-1 may be an effective method for the treatment of nicotine-induced inflammatory factor expression in bronchial epithelial cells.
【学位授予单位】：山东大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R363
【共引文献】
相关期刊论文 前1条
1 霍清伟;李东风;龙程;;多聚二磷酸腺苷聚合酶1与动脉粥样硬化[J];生物化学与生物物理进展;2012年05期
相关硕士学位论文 前10条
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8 黎明;PARP抑制对小鼠结肠癌CT26细胞侵袭影响及其机制探讨[D];重庆医科大学;2008年
9 李娟;氯化钠抑制内皮型一氧化氮合成酶活性及其机制探讨[D];泰山医学院;2008年
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