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首页> 外文期刊>Cell biochemistry and function >Recuperating lung decoction attenuates inflammation and oxidation in cigarette smoke-induced COPD in rats via activation of ERK and Nrf2 pathways
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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

机译:通过ERK和NRF2途径激活,恢复肺汤衰减在大鼠烟雾诱导的COPD中的炎症和氧化

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摘要

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-1 beta, IL-6, TNF-alpha, and TGF-beta 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.
机译:氧化/抗氧化不平衡和慢性炎症是慢性阻塞性肺病发病机制(COPD)的主要贡献。该研究评估了恢复肺汤(RLD)对由香烟烟雾和脂多糖(LPS)诱导的COPD诱导的大鼠炎症和氧化应激的影响。我们使用LPS的静脉内输注结合香烟烟雾暴露作为COPD大鼠模型。我们观察到RLD治疗增加了GSH的蛋白质水平和GSH / GSSG的比例,但血清中的8 OHDG和4-HNE。此外,RLD显着抑制了由香烟烟雾暴露引起的IL-1β,IL-6,TNF-α和TGF-β的表达,减少了支气管肺泡灌洗液中炎性细胞的数量,并减轻了卷烟烟雾的严重程度 - 引起的肺气肿。机械地,RLD处理通过磷酸化-ERK和NRF2表达的下调来预防疾病,该表达调节促炎细胞因子的产生。 RLD治疗对COPD施加了戏剧性的治疗效果。本研究揭示了一种机制,RLD函数对ERK信号传导来抑制炎症的调节。

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