Resolvin-D1 inhibits interleukin-8 and hydrogen peroxide production induced by cigarette smoke extract in 16HBE cells via attenuating NF-κB activation  

作　　者：Dong Jiajia Zhang Mingke Liao Zenglin Wu Wei Wang Tao Chen Lei Yang Ting Guo Lingli Xu Dan Wen Fuqiang 

机构地区：[1]Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China and Department of Respiratory Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China [2]Department of Hospital Internal Medicine, Northwest A&F University, Yangling, Shaanxi 712100, China

出　　处：《Chinese Medical Journal》2014年第3期511-517,共7页中华医学杂志（英文版）

基　　金：This study was supported by grants from the National Natural Science Foundation of China and China Medical Board of New York to Dr.Wen Fuqiang （No.31171103,No.81230001 and No.06834）.

摘　　要：Background Cigarette smoke induced airway inflammation plays a role in pathogenesis of airway inflammation.Resolvin-D1 derived from omega-3 polyunsaturated fatty acids is an endogenous anti-inflammatory and proresolving lipid mediator.Resolvin-D1 ameliorated inflammatory responses in lung injury,asthma,peritonitis and atherosclerosis.We investigated whether resolvin-D1 suppressed the productions of chemokines and oxidative stress induced by cigarette smoke extract （CSE） in vitro and its possible mechanism.Methods We examined the proinfiammatory chemokine interleukin-8 and hydrogen peroxide （H2O2）productions induced by CSE in 16 human bronchial epithelial （16HBE）cells after resolvin-D1 treatment and their mechanisms.16HBE cells were treated with resolvin-D1 at up to 10 nmol/L,for 30 minutes before CSE up to 16％ （v/v） exposure.Release of interlukin-8 proteins was assessed by enzyme linked immunosort assay （ELISA） and its mRNA level by RT-PCR.We evaluated extracellular H2O2 expression in the supematant.Phosphorylation of NF-KB/p65 and degradation of Ⅰ-KB in 16HBE cells were determined by Westem blotting analysis and NF-KB DNA binding activity by electrophoretic mobility shift assay （EMSA）.Results 16HBE cells treated with 8％ CSE showed significantly higher interlukin-8 production.Resolvin-D1 pretreatment inhibited CSE induced intedukin-8 production （mRNA and protein） in a dose and time dependent manner.Extracellular H2O2 level decreased after resolvin-D1 treatment.Resolvin-D1 attenuated CSE triggered Ⅰ-KB degradation and NF-KB/p65 activation dose dependently and inhibited NF-KB DNA binding activity.Conclusion Resolvin-D1 inhibits CSE induced interlukin-8 and H2O2 production in 16HBE cells by modulating NF-KB activation and has therapeutic potential for pulmonary inflammation.Background Cigarette smoke induced airway inflammation plays a role in pathogenesis of airway inflammation.Resolvin-D1 derived from omega-3 polyunsaturated fatty acids is an endogenous anti-inflammatory and proresolving lipid mediator.Resolvin-D1 ameliorated inflammatory responses in lung injury,asthma,peritonitis and atherosclerosis.We investigated whether resolvin-D1 suppressed the productions of chemokines and oxidative stress induced by cigarette smoke extract （CSE） in vitro and its possible mechanism.Methods We examined the proinfiammatory chemokine interleukin-8 and hydrogen peroxide （H2O2）productions induced by CSE in 16 human bronchial epithelial （16HBE）cells after resolvin-D1 treatment and their mechanisms.16HBE cells were treated with resolvin-D1 at up to 10 nmol/L,for 30 minutes before CSE up to 16％ （v/v） exposure.Release of interlukin-8 proteins was assessed by enzyme linked immunosort assay （ELISA） and its mRNA level by RT-PCR.We evaluated extracellular H2O2 expression in the supematant.Phosphorylation of NF-KB/p65 and degradation of Ⅰ-KB in 16HBE cells were determined by Westem blotting analysis and NF-KB DNA binding activity by electrophoretic mobility shift assay （EMSA）.Results 16HBE cells treated with 8％ CSE showed significantly higher interlukin-8 production.Resolvin-D1 pretreatment inhibited CSE induced intedukin-8 production （mRNA and protein） in a dose and time dependent manner.Extracellular H2O2 level decreased after resolvin-D1 treatment.Resolvin-D1 attenuated CSE triggered Ⅰ-KB degradation and NF-KB/p65 activation dose dependently and inhibited NF-KB DNA binding activity.Conclusion Resolvin-D1 inhibits CSE induced interlukin-8 and H2O2 production in 16HBE cells by modulating NF-KB activation and has therapeutic potential for pulmonary inflammation.

关 键 词：RESOLVINS airway inflammation oxidative stress INTERLEUKIN-8 NF-ΚB 

分 类 号：R562[医药卫生—呼吸系统]