[1]高云,陈玉,喻花平,等.巨噬细胞迁移抑制因子通过活性氧介导的有氧糖酵解促进肺纤维化[J].南方医科大学学报,2018,(07):873.
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巨噬细胞迁移抑制因子通过活性氧介导的有氧糖酵解促进肺纤维化()
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《南方医科大学学报》[ISSN:1673-4254/CN:44-1627/R]

卷:
期数:
2018年07期
页码:
873
栏目:
出版日期:
2018-06-30

文章信息/Info

Title:
Macrophage migration inhibitory factor promotes lung fibrosis via reactive oxygen species-mediated up-regulation of aerobic glycolysis
作者:
高云陈玉喻花平蓝海兵
关键词:
巨噬细胞迁移抑制因子肺纤维化有氧糖酵解活性氧族
Keywords:
macrophage migration inhibitory factor lung fibrosis aerobic glycolysis reactive oxygen species
摘要:
目的探讨巨噬细胞迁移抑制因子(MIF)在肺纤维发生发展的作用和机制。方法20只小鼠被随机分为对照组和肺纤维 化模型组,其中模型组气管内滴入博来霉素,30 d后检测肺组织中MIF的水平。用重组人MIF(rMIF)刺激人胚肺成纤维细胞 (HLF)细胞,观察活性氧、有氧糖酵解和胶原生成的水平;用活性氧抑制剂、有氧糖酵解抑制剂后,观察rMIF对胶原生成的影 响。结果小鼠肺纤维化肺组织和肺泡灌洗液中MIF水平较对照组显著升高(P<0.05)。rMIF可诱导活性氧、有氧糖酵解和胶原增 加,并随着rMIF的浓度升高而增加(P<0.05)。抑制活性氧后,可抑制rMIF和过氧化氢诱导的有氧糖酵解和胶原增加;抑制有氧 糖酵解后,可减少rMIF和活性氧诱导的胶原增加(P<0.05)。结论rMIF参与肺纤维发生发展,其机制可能是通过活性氧上调成 纤维细胞有氧糖酵解,促进胶原生成。
Abstract:
Objective To explore the role of macrophage migration inhibitory factor (MIF) in lung fibrosis and the possible molecular pathways involved. Methods Twenty male adult mice were randomized into control group and pulmonary fibrosis model group to receive intratracheal instillation of normal saline and bleomycin, respectively. Thirty days after the instillation, the level of MIF in the lung tissue of the mice was measured. Human embryonic lung fibroblasts (HLFs) were stimulated with recombinant human MIF (rMIF) and the changes in reactive oxygen species (ROS) levels, aerobic glycolysis and collagen production were measured; the effects of ROS inhibitor and glycolysis inhibitor on collagen productions were tested in rMIFstimulated HLF cells. Results Compared with the control mice, the mice with bleomycin-induced lung fibrosis exhibited significantly increased levels of MIF in the lung tissue and bronchoalveolar lavage fluid (BALF). ROS levels, aerobic glycolysis and collagen production were all increased in HLFs in response to rMIF stimulation; the enhancement of aerobic glycolysis and collagen production induced by rMIF and hydrogen peroxide were obviously suppressed by ROS inhibitor; the application of glycolysis inhibitor obviously inhibited rMIF-and hydrogen peroxide-induced increase of collagen production in HLFs. Conclusion rMIF participates in the development of pulmonary fibrosis in mice probably by up-regulating aerobic glycolysis via ROS to promote collagen production in fibroblasts.

相似文献/References:

[1]董昭兴,康庆鑫,雷雯,等.IL-17对肺成纤维细胞的增殖、转化和胶原合成作用[J].南方医科大学学报,2012,(01):75.
[2]李小溪,常红恩,奈文青,等.成纤维细胞生长因子受体各亚型与小鼠肺纤维化及衰老的关系[J].南方医科大学学报,2013,(04):607.

更新日期/Last Update: 1900-01-01