Recuperating lung decoction attenuates inflammation and oxidation in cigarette smoke‐induced COPD in rats via activation of ERK and Nrf2 pathways. (27th July 2017)

• Record Type: Journal Article
• Authors: Li, Chunlei; Yan, Yue; Shi, Qi; Kong, Yanhua; Gao, Longxia; Bao, Haipeng; Li, Youlin
• Is Part Of: Cell biochemistry and function. Volume 35:Number 5(2017)
• Page Start: 278
• Page End: 286
• Publication Date: 2017-07-27
• Subjects: COPD -- ERK/Nrf2 signalling pathway -- inflammation -- oxidative stress; Cytochemistry -- Periodicals; Cell metabolism -- Periodicals; Biochemistry -- Periodicals; Cytology -- Periodicals; 572
• DOI: 10.1002/cbf.3273
• Languages: English
• ISSNs: 0263-6484

Abstract

Abstract : 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.