Three Tiaobu Feishen formulae reduces cigarette smoke-induced inflammation in human airway epithelial cells  

作　　者：Dong Haoran Liu Xuefang Zheng Wanchun Feng Suxiang Li Jiansheng Qin Yanqin Wu Yaosong Chen Yulong Yin Sugai Zhao Peng 

机构地区：[1]Henan Key Laboratory of Chinese Medicine for Respiratory Disease,Henan University of Chinese Medicine,Zhengzhou 450046,China [2]Collaborative Innovation Center for Respiratory Disease Diagnosis and Treatment&Chinese Medicine Development of Henan Province,Henan University of Chinese Medicine,Zhengzhou 450046,China

出　　处：《Journal of Traditional Chinese Medicine》2020年第3期386-392,共7页中医杂志（英文版）

基　　金：Supported by National Natural Science Fund of China(No.81130062,81603473,81403367);Outstanding Traditional Chinese Medicine Academic Leader Program of Henan Province(No.HNZYLJ201301001);the National Key Technology R&D Program during the 12th Five-Year Plan Period(No.2014BAI10B06)。

摘　　要：OBJECTIVE: To investigate the therapeutic efficacy of Tiaobu Feishen formulae(TBFS) on cigarette smoke-induced inflammation in vitro using lipopolysaccharide(LPS)-induced and cigarette smoke extract(CSE)-induced NCI-H292 cells.METHODS: We evaluated the inhibitory effects of Bufei Jianpi formula(BJF), Bufei Yishen formula(BYF), and Yiqi Zishen formula(YZF) on the expressions of inflammatory cytokines including tumor necrosis factor(TNF)-α and interleukin(IL)-8, matrix metalloproteinase(MMP)-9, tissue inhibitor of matrix metalloprotease(TIMP)-1, and superoxide dismutase(SOD) in H292 cells stimulated with LPS or CSE. Their related transcription factors and signaling pathways were also analyzed.RESULTS: BJF, BYF, and YZF significantly inhibited the LPS-or CSE-induced expressions of TNF-α, IL-8,MMP-9, TIMP-1, and SOD in H292 cells, and suppressed the activation of transcription factors including nuclear transcription factor(NF)-κB, activator protein(AP)-1, and signal transducers and activators of transcription(STAT) 3 and their corresponding pathways, including NF-κB, mitogen-activated protein kinase(MAPK), STAT3, and peroxisome proliferator-activated receptor(PPAR).CONCLUSION: BJF, BYF, and YZF effectively suppressed inflammatory responses, protease-antiprotease imbalance, and oxidative stress induced by LPS and CSE, an effect that was closely associated with the inhibition of the NF-κB, MAPK, STAT3, and PPAR pathways.

关 键 词：Pulmonary disease chronic obstructive LIPOPOLYSACCHARIDES Cigarette smoking INFLAMMATION Epithelial cells Tiaobu Feishen formulae 

分 类 号：R285.5[医药卫生—中药学]