ABCA1
慢性阻塞性肺病
药理学
异硫氰酸烯丙酯
炎症
医学
姜黄素
化学
生物化学
免疫学
内科学
基因
运输机
作者
Wentao Zhu,Chenhui Li,Tingting Dai,Fu-Lin Tao,Mengwen Wang,Chong-Yang Wang,Zhili Han,Nianxia Sun,Yanan Zhao,Dianlei Wang
标识
DOI:10.1016/j.intimp.2021.108373
摘要
Allyl isothiocyanate(AITC) has been shown to play an important role in the improved symptoms of chronic obstructive pulmonary disease(COPD) and the inhibition of inflammation, but the role in COPD lipid metabolism disorder and the molecular mechanism remains unclear. We aimed to explore whether and how AITC affects COPD by regulating lipid metabolism and inflammatory response.The COPD rat model was established by cigarette smoke exposure. Cigarette smoke extract stimulated 16HBE cells to induce a cell model. The effect of AITC treatment was detected by lung function test, H&E staining, Oil red O staining, immunohistochemistry, ELISA, CCK-8, HPLC, fluorescence efflux test, siRNA, RT-PCR, and Western blotting. Biological analysis was performed to analyze the results. Graphpad Prism 8.0 software was used for statistical analysis.AITC can improve lung function and pathological injury in COPD rats. The levels of IL-1 β and TNF- α in the AITC treatment group were significantly lower than those in the model group(P < 0.05), and the lipid metabolism was also improved (P < 0.05). AITC reverses CSE-induced down-regulation of LXR α, ABCA1, and ABCG1 expression and function in a time-and concentration-dependent manner (P < 0.05). AITC regulates the cholesterol metabolism disorder induced by CSE in NR8383 cells and attenuates macrophage inflammation (P < 0.05). In addition, after silencing LXR α with siRNA, the effect of AITC was also inhibited.These results suggest that AITC improves COPD by promoting RCT process and reducing inflammatory response via activating LXR pathways.
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