[1]朱涛,施婵妹,李鹤,等.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[J].南方医科大学学报,2018,(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()
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《南方医科大学学报》[ISSN:1673-4254/CN:44-1627/R]

卷:
期数:
2018年10期
页码:
1209
栏目:
出版日期:
2018-10-16

文章信息/Info

Title:
Curcumin suppresses cigarette smoke extract-induced oxidative stress through PPARγ/ NF-κB pathway in human bronchial epithelial cells in vitro
作者:
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
关键词:
CSE16HBE细胞氧化应激PPARγNF-κB
Keywords:
cigarette smoke extract bronchial epithelial cells 16HBE cells oxidative stress PPARγ nuclear factor-κB
DOI:
10.12122/j.issn.1673-4254.2018.10.09
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.
更新日期/Last Update: 1900-01-01