Nucleosides isolated from <em>Ophiocordyceps sinensis</em> inhibit cigarette smoke extract-induced inflammation via the SIRT1–nuclear factor-κB/p65 pathway in RAW264.7 macrophages and in COPD mice

作者：Xiao Sun, Zhonghua Dong, Nan Li, Xiuli Feng, Yan Liu, Ang Li, Xiaosong Zhu, Chunyan Li, Zhongxi Zhao · 发表于：International Journal of COPD · 年份：2018 · DOI：10.2147/copd.s172579 · 被引用次数：46 · 研究领域：Fungal Biology and Applications、Genomics, phytochemicals, and oxidative stress、Seaweed-derived Bioactive Compounds

Background: Ophiocordyceps sinensis ( C. sinensis ) extracts have been found to have a therapeutic effect on patients with chronic obstructive pulmonary disease (COPD). Silent information regulator 1 (SIRT1) plays an important role in the regulation of inflammatory mediators and correlates with lung function and COPD exacerbations. The objective of this work was to explore the anti-inflammatory effect and preliminary pathways of nucleosides from cultured C. sinensis on RAW264.7 macrophages and COPD mice. Materials and methods: The nucleosides were extracted from cultured C. sinensis powder and further purified by macroporous resin D101 and glucan G10 columns. Inflammation and oxidative stress models in RAW264.7 macrophages and in mice were established by injection of cigarette smoke extract (CSE). We then examined how the isolated nucleosides regulated the production of the associated inflammatory mediators in vitro and in vivo by enzyme-linked immunosorbent assay, reverse transcription polymerase chain reaction, and Western blot. Results: The nucleosides inhibited inflammatory mediator expression of tumor necrosis factor-α, interleukin-6, interleukin-1β, and nitric oxide in both the CSE-stimulated RAW264.7 macrophages and mice. Moreover, the nucleosides elevated SIRT1 activation and suppressed nuclear factor-κB (NF-κB)/p65 activation in vitro and in vivo. Nucleoside treatment significantly decreased the levels of the inflammatory mediators in the bronchoalveolar lavage fluid...