Study on the effect of active components of Schisandra chinensis on liver injury and its mechanisms in mice based on network pharmacology

药物数据库 五味子 肝损伤 药理学 五味子 生物 系统药理学 计算生物学 维恩图 小桶 四氯化碳 药品 机制(生物学) 基因表达 中医药 基因 医学 生物化学 化学 基因本体论 四氯化碳 有机化学 替代医学 数学教育 病理 哲学 认识论 数学
作者
Guangyu Xu,Xi Lv,Yanbo Feng,Han Li,Cong Chen,Hao Lin,He Li,Chunmei Wang,Jianguang Chen,Jinghui Sun
出处
期刊:European Journal of Pharmacology [Elsevier BV]
卷期号:910: 174442-174442 被引量:16
标识
DOI:10.1016/j.ejphar.2021.174442
摘要

The aim of this study was to analyze the active components of Schisandra chinensis on liver injury and its mechanism in mice by network pharmacology. The active components of S. chinensis were found through Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and their corresponding targets were predicted. The targets of liver injury were searched through Therapeutic Targets Database (TTD), DisGeNET and drugbank databases, and the Venn diagram was constructed to obtain the action targets. The "drug-active component-target" network and protein-protein interaction network (PPI) were constructed by using STRING database and Cytoscape software, and the key targets were further screened by the enrichment analysis of relevant KEGG pathways. Finally, a CCl4-induced mouse liver injury model was established to verify the efficacy and related targets of S. chinensis and clarify its mechanism. Eight active components and 56 related targets of S. chinensis were screened out based on their oral bioavailability (OB) and drug likeness (DL). Five targets of S. chinensis related to liver injury were found by using the Venn diagram. The key targets, namely Ptgs2 and Nos2 genes, were further screened out by constructing a PPI network, and Schisandrol B (SCB) was considered the key component most closely related to the liver injury in S. chinensis. The results indicate that SCB may play a role in the treatment of the CCl4-induced liver injury by down-regulating the expression of iNOS and COX-2, and regulating the expression of NF-κB and IL-17 signaling pathway to inhibit the expression of proinflammatory factors.
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