中国药物警戒 ›› 2016, Vol. 13 ›› Issue (2): 74-77.

• 基础研究 • 上一篇    下一篇

苦参素涂膜剂对裸鼠增生性瘢痕作用及TGF-β/Smad信号通路调控

王爱丽, 顾耀辉, 黄静, 贾卿, 陈波, 徐顺*   

  1. 上海市第七人民医院烧伤整形科,上海 200137
  • 收稿日期:2016-03-14 修回日期:2016-03-14 出版日期:2016-02-08 发布日期:2016-03-14
  • 通讯作者: 徐顺,男,本科,主治医师,皮肤与烧伤整形科临床。E-mail:xushun197901@163.com。
  • 作者简介:王爱丽,女,硕士,主治医师,皮肤与烧伤整形科临床。
  • 基金资助:
    上海市浦东新区卫生局面上项目(PW2013A-25); 上海市中医、中西医结合临床重点扶持项目(ZY3-JSFC-1-1014)

Effects of Kushenin Pellicle on Hypertrophic Scar and TGF-β/Smad Signal Transduction Pathway

WANG Ai-li, GU Yao-hui, HUANG Jing, JIA Qing, CHEN Bo, XU Shun*   

  1. Burn Unit of Shanghai Seventh People’s Hospital, Shanghai 200137, China
  • Received:2016-03-14 Revised:2016-03-14 Online:2016-02-08 Published:2016-03-14

摘要: 目的探讨苦参素对裸鼠增生性瘢痕的抑制作用及其有效作用机制,为该药的临床应用提供理论依据。方法用人源增生性瘢痕移植方法,制备增生性瘢痕裸鼠模型,术后10 d,裸鼠30只,随机分为模型组、苦参素涂膜剂组、阳性药组,药物组分别涂抹苦参素涂膜剂和阳性药,每天2次,连续8周;对照组涂抹基质。每周观察并拍照记录瘢痕的生长情况,于术后10、35、49、56 d测量瘢痕面积, RT-PCR检测组织中的TGF-β1、Smad3的表达, Western-blot方法检测TGF-β1和Smad3蛋白的表达。结果模型对照组瘢痕生长较快,愈合较慢,阳性药和苦参素涂膜剂组,瘢痕生长显著被抑制,随着用药时间的延长,其抑制作用明显增强。与模型对照组相比,苦参素涂膜剂组的TGF-β1、Smad3 mRNA和蛋白的表达量明显下降。结论苦参素涂膜剂能抑制增生性瘢痕的生长并下调TGF-β1、Smad3 mRNA和蛋白的表达,调控TGF-β/Smad信号通路表达可能是苦参素抑制增生性瘢痕的机制之一。

关键词: 苦参素, 涂膜剂, 增生性瘢痕, 转化生长因子β, 1, Smad3

Abstract: ObjectiveTo investigate the effects of kushenin on hypertrophic scar and its effective mechanism. MethodsHuman hypertrophic scar tissues were subcutaneously transplanted into the back of 30 nude mice to create the animal models of hypertrophic scar. Ten days after the operation, the mice were distributed into the model control, kushenin pellicle and positive medicine group. Drugs were applied 2 times a day for 8 weeks. The growth of the scar was observed and photographed every week, and its size was measured after 10, 35, 49 and 56 d. RT-PCR and Western Blot assessment was used to detect the mRNA and protein expression of TGF-β1 and Smad3. ResultsThe growth of scars in the model control group was more rapid than that of the kushenin pellicle and positive medicine treatment group. The inhibition effect became more obvious with extended medication time. Compared with the model control group, the mRNA and protein expression of TGF-β1 and Smad3 were declined sharply in kushenin pellicle group. ConclusionThe mechanisms of anti-hypertrophic scar effects of kushenin maybe involve inhibiting the TGF-β/Smad signal transduction pathway.

Key words: kushenin, pellicle, hypertrophic scar, TGF-β1, Smad3

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