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基于网络药理学方法探索益肺散结方治疗肺纤维化的潜在机制

A Network Pharmacology Approach to Explore the Potential Mechanisms of Yifei Sanjie Formula in Treating Pulmonary Fibrosis.

作者信息

Qiao Bo, Wu Yueying, Li Xiaoya, Xu Zhenyuan, Duan Weigang, Hu Yanan, Jia Wenqing, Fan Qiuyang, Xing Haijing

机构信息

School of Basic Medical Science, Yunnan University of Chinese Medicine, Kunming, Yunnan, China.

College of First Clinical Medical Science, Yunnan University of Chinese Medicine, Kunming, Yunnan, China.

出版信息

Evid Based Complement Alternat Med. 2020 Nov 30;2020:8887017. doi: 10.1155/2020/8887017. eCollection 2020.

DOI:10.1155/2020/8887017
PMID:33335558
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7722457/
Abstract

OBJECTIVE

Yifei Sanjie Formula (YFSJF) is an effective formula on pulmonary fibrosis (PF), which has been used in clinic for more than 30 years. In order to investigate the molecular mechanism of YFSJF in treating PF, network pharmacology was used to predict the cooperative ingredients and associated pathways.

METHODS

Firstly, we collected potential active ingredients of YFSJF by TCMSP databases. Secondly, we obtained PF-associated targets through OMIM and Genecards database. Finally, metascape was applied for the analysis of GO terms and KEGG pathways.

RESULTS

We screened out 76 potential active ingredients and 98 associated proteins. A total of 5715 items were obtained by GO enrichment analysis ( < 0.05), including 4632 biological processes, 444 cellular components, and 639 molecular functions. A total of 143 related KEGG pathways were enriched ( < 0.05), including IL-17 signaling pathway, T cell receptor signaling pathway, TNF signaling pathway, calcium signaling pathway, TH17 cell differentiation, HIF-1 signaling pathway, and PI3K-Akt signaling pathway.

CONCLUSION

YFSJF can interfere with immune and inflammatory response through multiple targets and pathways, which has a certain role in the treatment of PF. This study lays a foundation for future experimental research.

摘要

目的

益肺散结方（YFSJF）是治疗肺纤维化（PF）的有效方剂，已在临床应用30余年。为探讨益肺散结方治疗PF的分子机制，采用网络药理学方法预测协同成分及相关通路。

方法

首先，通过中药系统药理学数据库与分析平台（TCMSP）收集益肺散结方潜在活性成分。其次，通过在线人类孟德尔遗传数据库（OMIM）和基因卡片数据库（Genecards）获取PF相关靶点。最后，运用Metascape进行基因本体（GO）术语和京都基因与基因组百科全书（KEGG）通路分析。

结果

筛选出76种潜在活性成分和98种相关蛋白。通过GO富集分析共获得5715项（<0.05），包括4632个生物学过程、444个细胞组分和639个分子功能。共富集到143条相关KEGG通路（<0.05），包括白细胞介素-17信号通路、T细胞受体信号通路、肿瘤坏死因子信号通路、钙信号通路、辅助性T细胞17（TH17）细胞分化、缺氧诱导因子-1（HIF-1）信号通路和磷脂酰肌醇-3激酶-蛋白激酶B（PI3K-Akt）信号通路。

结论

益肺散结方可通过多个靶点和通路干预免疫和炎症反应，对PF治疗具有一定作用。本研究为今后的实验研究奠定了基础。

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