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目的通过检测尼古丁刺激的支气管上皮细胞中炎症因子的变化,探讨聚二磷酸腺苷核糖聚合酶1(PARP1)在Toll样受体4(TLR4)介导的炎症中的作用和机制。方法培养支气管上皮细胞。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性一氧化氮合酶(iNOS)、细胞间黏附分子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。结论尼古丁刺激通过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。在支气管上皮不典型增生中,PARP-1抑制或许是降低轻尼古丁诱导的炎症因子表达的有效手段。
Objective To investigate the role and mechanism of PARP1 in Toll-like receptor 4 (TLR4) -mediated inflammation by detecting the changes of inflammatory cytokines in nicotine-stimulated bronchial epithelial cells. Methods Culture bronchial epithelial cells. The expressions of inflammatory cytokines and proteins in the nicotine-stimulated group and the negative control group, the TLR4 and PARP1 inhibitory groups, and the negative control group were detected. Results Compared with the control group, nicotine stimulation increased the protein expression of TLR4 and PARP1. TLR4 inhibition reduced nicotine-induced up-regulation of inducible nitric oxide synthase (iNOS), intercellular adhesion molecule-1 (ICAM-1) and PARP1. Inhibition of nuclear factor kappa B reduces the expression of iNOS and ICAM-1. Inhibition of PARP1 reduces nicotine-induced inflammatory factor expression by preventing nuclear translocation of NF-κB. Conclusion Nicotine can stimulate the expression of ICAM-1 and iNOS through the TLR4 / PARP1 / NF-κB pathway. PARP-1 may be an indispensable factor in nicotine-induced, TLR4-mediated inflammation. In bronchial epithelial dysplasia, PARP-1 inhibition may be an effective means of reducing the expression of the light nicotine-induced inflammatory cytokines.