生物技术进展 ›› 2017, Vol. 7 ›› Issue (5): 501-505.DOI: 10.19586/j.2095-2341.2017.0064

• 硒与健康 • 上一篇    下一篇

硒在地方病中的防治作用及其分子机制研究进展

熊咏民,杨晓莉,张荣强,李宝荣,陈静宏,代晓霞,陈群,谭武红,张峰   

  1. 西安交通大学医学部公共卫生学院地方病研究所, 国家卫计委微量元素与地方病重点实验室, 西安 710061
  • 收稿日期:2017-06-21 出版日期:2017-09-25 发布日期:2017-07-13
  • 通讯作者: 熊咏民,教授,主要从事微量元素与地方病关系研究。E-mail:xiongym@mail.xjtu.edu.cn
  • 作者简介:熊咏民,教授,主要从事微量元素与地方病关系研究。E-mail:xiongym@mail.xjtu.edu.cn
  • 基金资助:
    国家自然科学基金项目(81573104;81172610;81673117;81673115)资助。

The Effect of Selenium on Endemic Diseases and its Molecular Mechanism

XIONG Yongmin, YANG Xiaoli, ZHANG Rongqiang, LI Baorong, CHEN Jinghong, DAI Xiaoxia, CHEN Qun, TAN Wuhong, ZHANG Feng   

  1. Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, Institute of Endemic Diseases, School of Public Health, Xi'an Jiaotong University Health Science Center, Xian 710061, China
  • Received:2017-06-21 Online:2017-09-25 Published:2017-07-13

摘要: 大骨节病、克山病、地方性氟中毒和地方性砷中毒是我国的主要地方病,其病因、发病机制均与宏量元素和微量元素的缺乏、中毒与失衡有关。低硒是大骨节病和克山病的重要环境因素,补硒对其具有一定防治效果。综述了微量元素硒与大骨节病和克山病之间的关系,以及硒元素在大骨节病、克山病、氟中毒和硒中毒中的作用机制方面的研究进展,旨在进一步探索微量元素硒的生物学潜能及其分子机制,更好地造福于人类。

关键词: 硒, 地方病, 细胞凋亡, 信号转导, 氧化应激

Abstract: The main endemic diseases in our country include Kashin-beck disease, Keshan disease, endemic fluorosis and arseniasis. Their etiology and pathogenesis refer to the deficiency, toxicity and imbalance of macroelement and microelement. The selenium (Se) deficiency is the important environmental factor for Kashin-beck disease and Keshan disease, and Se supplement has good effects of prevention and treatment on Kashin-beck disease and Keshan disease. This article summarized the progress on relationship between Se and Kashin-beck disease and Keshan disease, and the action mechanism of Se in Kashin-beck disease, Keshan disease, endemic fluorosis and arseniasis. The paper was aimed to explore the potential biological functions and molecular mechanisms of Se, which was expected to bring benefits to mankind preferably.

Key words: selenium, endemic diseases, cell apotosis, signal transduction, oxidative stress