国际口腔医学杂志 ›› 2020, Vol. 47 ›› Issue (6): 732-738.doi: 10.7518/gjkq.2020089

• 综述 • 上一篇    下一篇

茶多酚类化合物在牙本质粘接中应用的研究进展

刘恩言(),李明云()   

  1. 口腔疾病研究国家重点实验室 国家口腔疾病临床医学研究中心 四川大学华西口腔医学院 成都 610041
  • 收稿日期:2020-02-05 修回日期:2020-05-28 出版日期:2020-11-01 发布日期:2020-11-06
  • 通讯作者: 李明云
  • 作者简介:刘恩言,学士,Email: liuenyanAPTX@163.com
  • 基金资助:
    国家自然科学基金青年项目(81400501)

Research progress on tea polyphenols in dentin adhesion

Liu Enyan(),Li Mingyun()   

  1. State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & West China School of Stomatology, Sichuan University, Chengdu 610041, China
  • Received:2020-02-05 Revised:2020-05-28 Online:2020-11-01 Published:2020-11-06
  • Contact: Mingyun Li
  • Supported by:
    Youth Program of National Natural Science Foundation of China(81400501)

摘要:

牙体粘接技术历经多代改良,目前广泛用于口腔缺损修复领域。虽然牙体粘接技术可以满足更保守的临床治疗要求,但随着时间的推移,牙本质-粘接剂形成的粘接界面会发生退化,目前这仍然是一个热点问题。茶多酚类化合物结构中含多个酚羟基,易与牙本质胶原分子形成氢键,从而改善树脂牙本质粘接修复的耐久性。近年来,有关茶多酚类化合物中的主要活性物质表没食子儿茶素没食子酸酯(EGCG)加入牙本质粘接剂中对于牙本质粘接效果的影响以及作用机制成为研究热点,本文就茶多酚中主要活性物质EGCG在牙本质粘接过程中发挥的作用以及相应机制作一综述。

关键词: 茶多酚类化合物, 表没食子儿茶素-3-没食子酸酯, 牙本质粘接体系, 粘接剂, 基质金属蛋白酶

Abstract:

The technology of tooth bonding is improved for many generations and is widely used in the field of oral defect repair. The dental adhesive technique can meet the conservative clinical treatment requirements, but the issue that the dentin-adhesive interface deteriorates over time remains. The structure of tea polyphenols contains multiple phenolic hydroxyl groups, which easily form hydrogen bonds with dentin collagen molecules, thereby improving the durability of the resin dentin adhesion repair. In recent years, the effects of the addition of epigallocatechin-3-gallate (EGCG), the main active substance in tea polyphenols, on the dentin bonding effect and the mechanism of action have become the research focus. In this paper, the role of EGCG in the dentin bonding process and the corresponding mechanism are reviewed.

Key words: tea polyphenols, epigallocatechin-3-gallate, dentin bonding system, bonding agent, matrix metalloproteinase

中图分类号: 

  • R783.1

表1

MMP降解牙本质胶原的分子机制"

亚类 分子机制
MMP-1、MMP-3、MMP-9 有研究[28]表明,人肝星状细胞高表达MMP-1后抑制Ⅰ型胶原蛋白表达的机制主要通过发挥其酶活性降解Ⅰ型胶原蛋白,而不影响Ⅰ型胶原基因水平的表达。
此外,研究证实激活蛋白1(activator protein-1,AP-1)在MMP-1、MMP-3和MMP-9的转录上调中起关键作用,MMP-1过表达导致Ⅰ型胶原纤维中心三螺旋内的特定位置开始裂解,一旦裂解,这些纤维被MMP-3和MMP-9进一步降解。
MMP-2 研究显示,MMP-2降解Ⅰ型胶原的表达涉及多个信号通路,包括环磷酸腺苷(cyclic adinosine monophosphate,cAMP)依赖蛋白激酶(protein kinaseA,PKA)、 AP-1、核因子κB(nuclear factor kappa-B,NF-κB)和丝裂原活化蛋白激酶(mitogen activated protein kinases,MAPK)家族等信号通路。Xie等[29]在研究中采用上述通路的抑制剂来观察通路抑制剂对激活的MMP-2在细胞外基质中的影响,结果显示6种抑制剂均在不同程度上降低MMP-2的表达或去除MMP-2的活性形式。
除了MMP-2可降解Ⅰ型胶原,Ⅰ型胶原也在MMP-2活化中起作用[30]。两者调控机制研究较多的是p38/细胞外调节蛋白激酶(extracellular regulated protein kinases,ERK)通路[31]。Koontongkaew等[32]的研究发现,Ⅰ型胶原可以通过ERK1/2、p38等通路活化MMP-2。
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