关键词: 支气管上皮细胞；炎症因子；Toll样受体4；聚二磷酸腺苷核糖聚合酶1；核因子κB；尼古丁

Abstract:

Objective   To detect the changes of bronchial epithelial cells inflammatory cytokine stimulated by nicotine and to investigate the function and mechanism of poly(ADP-ribose) polymerase 1 (PARP1) in the inflammatory response mediated by toll-like receptor 4 (TLR4). Methods   Bronchial epithelial cells were cultivated. The expressions of inflammatory cytokine-related gene and protein were detected in nicotine stimulation group, TLR4 and PARP1 inhibition group and their negative control groups. Results   Compared with the controls, nicotine stimulation increased the protein expressions of TLR4 and PARP1. TLR4 inhibition reduced nicotine-induced up-regulations of iNOS, ICAM-1 and PARP1. NF-κB inhibition decreased ICAM-1 and iNOS expressions. PARP1 inhibition decreased protein expression of inflammatory cytokines induced by nicotine stimulation, probably through preventing NF-κB nuclear translocation. Conclusion   Nicotine increases ICAM-1 and iNOS expressions via TLR4/PARP1/NF-κB pathway. PARP1 might be a dispensable factor in TLR4-mediated inflammation after nicotine stimulation. PARP1 inhibition might shed a light on the decrease of nicotine-induced inflammatory cytokines expression during bronchial epithelium atypical heperplasia.

Key words: Bronchial endothelial cells; Inflammatory cytokine; Toll-like receptor 4; Poly(ADP-ribose) polymerase 1; Nuclear factor-κB; Nicotine