Li Chunlei, Yan Yue, Shi Qi, Kong Yanhua, Gao Longxia, Bao Haipeng, Li Youlin
Beijing University of Chinese Medicine, Beijing, China.
The Key Institute of State Administration of Traditional Chinese Medicine (pneumonopathy chronic cough and dyspnea) Beijing Key Laboratory (No.BZ0321), China-Japan Friendship Hospital, Beijing, China.
Cell Biochem Funct. 2017 Jul;35(5):278-286. doi: 10.1002/cbf.3273.
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.
氧化/抗氧化失衡和慢性炎症是慢性阻塞性肺疾病（COPD）发病机制的主要促成因素。本研究评估了复肺汤（RLD）对香烟烟雾和脂多糖（LPS）诱导的COPD大鼠炎症和氧化应激的影响。我们采用静脉注射LPS联合香烟烟雾暴露建立COPD大鼠模型。我们观察到，RLD治疗可提高血清中谷胱甘肽（GSH）的蛋白水平和GSH/GSSG比值，但降低8-羟基脱氧鸟苷（8-OHdG）和4-羟基壬烯醛（4-HNE）水平。此外，RLD显著抑制香烟烟雾暴露诱导的白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）和转化生长因子-β（TGF-β）的表达，减少支气管肺泡灌洗液中炎症细胞数量，并减轻香烟烟雾诱导的肺气肿严重程度。机制上，RLD治疗通过下调磷酸化细胞外信号调节激酶（p-ERK）和核因子E2相关因子2（Nrf2）的表达来预防疾病，而p-ERK和Nrf2可调节促炎细胞因子的产生。RLD治疗对COPD具有显著的治疗作用。本研究揭示了RLD通过调节ERK信号通路抑制炎症的机制。
