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Recuperating lung decoction attenuates inflammation and oxidation in cigarette smoke‐induced COPD in rats via activation of ERK and Nrf2 pathways
Author(s) -
Li Chunlei,
Yan Yue,
Shi Qi,
Kong Yanhua,
Gao Longxia,
Bao Haipeng,
Li Youlin
Publication year - 2017
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.3273
Subject(s) - copd , bronchoalveolar lavage , inflammation , proinflammatory cytokine , oxidative stress , medicine , mapk/erk pathway , downregulation and upregulation , pathogenesis , lung , immunology , pharmacology , glutathione , endocrinology , chemistry , kinase , biochemistry , enzyme , gene
Oxidative/antioxidative imbalance and chronic inflammation are the main contributors to the pathogenesis of chronic obstructive pulmonary disease (COPD). This study evaluated the effect of recuperating lung decoction (RLD) on inflammation and oxidative stress in rats with COPD induced by cigarette smoke and lipopolysaccharides (LPS). We used intravenous infusion of LPS combined with cigarette smoke exposure as a COPD rat model. We observed that RLD treatment increased the protein level of GSH and the ratio of GSH/GSSG but decreased 8‐OHdG and 4‐HNE in the serum. Furthermore, RLD significantly inhibited the expressions of IL‐1β, IL‐6, TNF‐α, and TGF‐β induced by cigarette smoke exposure, reduced the number of inflammatory cells in the bronchoalveolar lavage fluid, and alleviated the severity of cigarette smoke‐induced emphysema. Mechanistically, RLD treatment prevented disease through downregulation of phosphorylated‐ERK and Nrf2 expression, which regulates the production of proinflammatory cytokines. RLD treatment exerted a dramatic therapeutic effect on COPD. This study revealed a mechanism that RLD functions on the regulation of ERK signalling to inhibit inflammation.