刘涛,宋良文,董俊兴,黄山英,李杨.二咖啡酰奎宁酸对小鼠肺纤维化的早期防治作用[J].中华放射医学与防护杂志,2005,25(1):36-39
二咖啡酰奎宁酸对小鼠肺纤维化的早期防治作用
Preventive and curative effects of dicaffeoylquinic acid on early pulmonary fibrosis in mice
投稿时间:2004-02-28  
DOI:
中文关键词:  二咖啡酰奎宁酸  α-平滑肌肌动蛋白  基质溶解素  肺纤维化  防治
英文关键词:Dicaffeoylquinic acid  α-smooth muscle actin  Matrilysin  Pulmonary fibrosis  Prevention and treatment
基金项目:军事医学科学开发研究基金资助项目(2002)
作者单位E-mail
刘涛 100850 北京, 军事医学科学院放射医学研究所 Lsong1.@yahoo.com 
宋良文 100850 北京, 军事医学科学院放射医学研究所  
董俊兴 100850 北京, 军事医学科学院放射医学研究所  
黄山英 100850 北京, 军事医学科学院放射医学研究所  
李杨 100850 北京, 军事医学科学院放射医学研究所  
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中文摘要:
      目的 探讨二咖啡酰奎宁酸(IBE5)对博莱霉素诱导的C57小鼠肺纤维化的防治作用及其机制。方法 分别进行羟脯氨酸(Hyp)检测、图像分析、Ⅰ和Ⅲ型胶原测定、α-平滑肌肌动蛋白(α-SMA)和基质溶解素(MMP7)免疫组织化学检测。结果 ①IBE5能降低纤维化肺组织内Hyp含量(P<0.05);②BLM组肺泡明显减少,间隔增宽,肺内胶原沉积和纤维化。IBE5能减轻肺泡破坏和纤维化(P<0.05);③BLM组肺间质合成大量Ⅰ、Ⅲ型胶原,IBE5治疗后胶原减少(P<0.05);④BLM组α-SMA增加,位于纤维化区的肌成纤维细胞中;MMP7免疫组织化学检测显示肌成纤维细胞阳性。应用IBE5后α-SMA、MMP7减少(P<0.05)。结论 IBE5通过抑制成纤维细胞向肌成纤维细胞转化和MMP7表达对肺纤维化具有防治作用。
英文摘要:
      Objective To explore the effect of dicaffeoylquinic acid(IBE5) on prevention and treatment of pulmonary fibrosis induced by bleomycin(BLM) in mice and its mechanism. Methods Hydroxyproline content determination,imaging analysis,collagen Ⅰand Ⅲ assay,α-smooth muscle actin(α-SMA) and matrix metalloproteinase 7(MMP-7) immunohistochemistry were performed. Results ①Hydroxyproline content decreased in fibrotic lung tissue after administration of IBE5(P<0.05).②The number of pulmonary alveoli reduced,alveolus interstitium was thickened and collagen deposition and fibrosis were formed in lung tissue of BLM group. The break of pulmonary alveoli and extension of pulmonary fibrosis were decreased by use of IBE5 (P<0.05).③A lot of collagen Ⅰand Ⅲ were synthesized in lung interstitium in BLM group and their quantity was reduced in IBE5 group (P<0.05).④In BLM group,α-SMA expression increased and located in myofibroblasts in fibrotic area,and MMP7 immunohistochemical signal was located in myofibroblasts also. They were decreased in IBE5 group(P<0.05). Conclusion IBE5 plays a preventive and curative role in pulmonary fibrosis by inhibition of transformation of fibroblasts towards myofibroblasts and MMP7 expression.
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