中国药物警戒 ›› 2021, Vol. 18 ›› Issue (8): 753-759.
DOI: 10.19803/j.1672-8629.2021.08.11

• 基础与临床研究 • 上一篇    下一篇

大黄素致结肠黑变病的机制研究与风险预警

黄政凯1, 林志健1,2,*, 王雨1, 郭凡帆1, 张冰1,2#   

  1. 1北京中医药大学中药学院,北京 100029;
    2北京中医药大学中药药物警戒与合理用药研究中心,北京 100029
  • 收稿日期:2020-05-22 出版日期:2021-08-15 发布日期:2021-08-17
  • 通讯作者: *林志健,博士,副教授·硕导,中药防治代谢性疾病研究,中药药物警戒与合理用药。E-mail: linzhijian83@126.com #为共同通信作者。
  • 作者简介:黄政凯,男,在读硕士,中药防治代谢性疾病研究、中药药物警戒与合理用药。
  • 基金资助:
    国家自然科学基金项目(81874349); 北京中医药大学基本科研业务费重点攻关项目课题(2020-JYB-ZDGG-036)

The research on Mechanism and Risk Warning of Melanosis Coli Caused by Emodin

HUANG Zhengkai1, LIN Zhijian1,2,*, WANG Yu1, GUO Fanfan1, ZHANG Bing1,2#   

  1. 1School of Chinese Pharmacy, Beijing University of Chinese Medicine, Beijing 100029, China;
    2Center for Pharmacovigilance and Rational Use of Chinese Medicine, Beijing 100029, China
  • Received:2020-05-22 Online:2021-08-15 Published:2021-08-17

摘要: 目的 探讨大黄素抑制巨噬细胞激活的机制,阐释其在结肠黑变病发生过程中的作用,明确大黄素诱发结肠黑变病的潜在风险。方法 采用生物信息学技术,对高通量基因表达数据库中有关大黄素抑制巨噬细胞激活的基因芯片GSE 73309和GSE 73310进行筛选分析,对差异表达基因进行基因本体论数据库功能注释、京都基因与基因组百科全书数据库通路分析及蛋白质互作网络分析。同时,通过检索大黄素临床应用与基础研究文献,挖掘大黄素致结肠黑变病的生物学基础,并与生物信息分析结果相互印证。结果 大黄素抑制巨噬细胞激活的生物途径主要体现在肿瘤坏死因子、缺氧诱导因子相关的炎症反应和癌症通路。结论 大黄素致结肠黑变病的机制与大黄素诱发的炎症反应密切相关。同时,大黄素具有诱发乳腺癌、卵巢癌以及肺部气道炎症反应的安全风险。

关键词: 大黄素, 结肠黑变病, 蒽醌类中药, 风险警戒

Abstract: Objective To explore the mechanism by which emodin inhibits macrophage activation, explain its role in the occurrence of melanosis coli, and find out about the potential risk of emodin induced melanosis coli. Methods Bioinformatics technology was used to screen and analyze the gene chips GSE 73309 and GSE 73310 related to inhibition of macrophage activation by emodin in GEO database. Gene Ontology(GO) annotation, Kyoto Encyclopedia of Genes Genomes (KEGG) pathway analysis, and Protein-protein interaction network analysis were performed on differentially expressed genes. By retrieving literature on clinical applications and basic research of emodin, the biological basis of rhubarb-induced melanosis coli was explored, and the results of biological information analysis were mutually confirmed. Results The biological pathways through which emodin inhibited macrophage activation were mainly manifested in inflammatory responses and cancer pathways related to tumor necrosis factors (TNF) and hypoxia inducible factors (HIF). Conclusion The mechanism by which emodin induces melanosis coli is closely related to the inflammatory reaction induced by emodin. In addition, emodin can potentially induce breast cancer, ovarian cancer and lung airway inflammation.

Key words: emodin, melanosis coli, anthraquinone traditional Chinese medicine, risk warning

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