南方医科大学学报

南方医科大学学报 ›› 2018, Vol. 38 ›› Issue (10): 1209-.doi: 10.12122/j.issn.1673-4254.2018.10.09

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姜黄素通过调控PPARγ/NF-κB信号通路减轻CSE诱导的人气道上皮细胞氧化应激反应

朱涛，施婵妹，李鹤，何婧，杨艳丽，王勤，邓欣雨，吴砚樵，王静，赵燕，邓火金   

  • 出版日期:2018-10-20 发布日期:2018-10-20

Curcumin suppresses cigarette smoke extract-induced oxidative stress through PPARγ/ NF-κB pathway in human bronchial epithelial cells in vitro

  • Online:2018-10-20 Published:2018-10-20

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摘要： 目的探讨姜黄素对香烟烟雾提取物（CSE）诱导的人气道上皮16HBE细胞氧化应激和炎症反应的抑制作用及相关的分子 机制。方法使用shRNA-PPARγ（shPPARγ）转染人气道上皮16HBE细胞下调PPARγ表达。将16HBE细胞分为5组即对照组、 姜黄素组、CSE组、CSE+姜黄素组和CSE+姜黄素+shRNA-PPARγ组。在0 h和24 h时使用MTT法对细胞活性进行检测；干预 24 h后使用qPCR对细胞TNF-α、iNOS和PPARγ mRNA表达进行检测，采用western blot检测16HBE细胞中iNOS、PPARγ蛋白 表达以及NF-κB p65磷酸化水平。结果16HBE细胞在干预24 h后各组之间细胞活性未有明显统计学差异（P>0.05）。与对照 组相比较，CSE干预24 h后PPARγ表达水平明显降低，TNF-α、iNOS表达及NF-κB p65磷酸化水平明显升高，差异均有统计学意 义（P<0.05）。但CSE组较CSE+姜黄素组和CSE+姜黄素+shPPARγ组PPARγ表达水平下降以及TNF-α、iNOS表达和NF-κB p65 磷酸化水平升高更显著，差异均有统计学意义（P<0.05）；且CSE+姜黄素+shPPARγ组较CSE+姜黄素组PPARγ表达水平下降以 及TNF-α、iNOS表达和NF-κB p65磷酸化水平升高更明显，差异均有统计学意义（P<0.05）。结论姜黄素可以通过抑制PPARγ/ NF-κB信号通路减轻CSE诱导的人气道上皮16HBE细胞的炎症反应及氧化应激。为姜黄素应用于慢性阻塞性肺疾病等疾病 的临床治疗奠定了理论基础。

Abstract: Objective To investigate the effect of curcumin against cigarette smoke extract (CSE)- induced oxidative stress in human bronchial epithelial cells and explore the underlying mechanism. Methods Human bronchial epithelial cell line 16HBE was treated for 24 h with curcumin, CSE, CSE + curcumin, and CSE + curcumin with transfection by a short hairpin RNA targeting PPARγ (shPPARγ). MTT assay was used to observe the changes in the cell viability after the treatments. Quantitative real-time PCR was performed to detect the mRNA expressions of tumor necrosis factor-α (TNF-α), iNOS and PPARγ in the cells, and the protein expressions of iNOS, PPARγ and the phosphorylation of NF-κB p65 were detected using Western blotting. Results The treatments did not cause significant changes in the cell viability. Exposure to CSE for 24 h significantly lowered PPARγ expression and increased TNF-α and iNOS expressions and phosphorylation of NF-κB p65 in the cells. The effects of CSE were significantly suppressed by curcumin, but transfection of the cells with shRNA-PPARγ obviously abrogated the suppressive effects of curcumin. Conclusions Curcumin suppresses CSE-induced oxidative stress and inflammation via the PPARγ/NF-κB signaling pathway in 16HBE cells, suggesting the potential of curcumin in the treatment of chronic obstructive pulmonary disease.