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Investigation of the active ingredients and mechanism of Shuangling extract in dextran sulfate sodium salt induced ulcerative colitis mice based on network pharmacology and experimental verification

作     者:CHU Mengzhen WANG Yu LIN Zhijian Lyu Jintao ZHANG Xiaomeng ZHANG Bing CHU Mengzhen;WANG Yu;LIN Zhijian;Lyu Jintao;ZHANG Xiaomeng;ZHANG Bing

作者机构:Department of Clinical Chinese PharmacySchool of Chinese Materia MedicaBeijing University of Chinese Medicine 

出 版 物:《Journal of Traditional Chinese Medicine》 (中医杂志(英文版))

年 卷 期:2024年第44卷第3期

页      面:478-488页

核心收录:

学科分类:1008[医学-中药学(可授医学、理学学位)] 1006[医学-中西医结合] 1002[医学-临床医学] 100602[医学-中西医结合临床] 10[医学] 

基  金:the Innovation Team and Talents Support Program of National Administration of Traditional Chinese Medicine:Construction and Practice of Pharmacovigilance Theory System in Line with the Characteristics of Traditional Chinese Medicine (No. ZYYCXTD-C-202005-11) the National Leading Talents Support Plan of Traditional Chinese Medicine 'Qihuang Scholar' Plan:Chinese Medicine Inheritance and Innovation "One Hundred Million" Talent Project (Qihuang Project) Qihuang Scholars (No. 1040063320004) 

主  题:Shuangling extract colitis, ulcerative molecular docking simulation network pharmacology pharmacodynamic study 

摘      要:OBJECTIVE: To explore the pharmacodynamic effects and potential mechanisms of Shuangling extract against ulcerative colitis(UC). METHODS: The bioinformatics method was used to predict the active ingredients and action targets of Shuangling extract against UC in mice. And the biological experiments such as serum biochemical indexes and histopathological staining were used to verify the pharmacological effect and mechanism of Shuangling extract against UC in mice. RESULTS: The Shuangling extract reduced the levels of seruminterleukin-1β(IL-1β), tumor necrosis factor-α(TNF-N), interleukin-6(IL-6) and other inflammatory factors in UC mice and inhibited the inflammatory response. AKT Serine/threonine Kinase 1 and IL-6 may be the main targets of the anti-UC action of Shuangling extract, and the TNF signaling pathway, Forkhead box O signaling pathway and T-cell receptor signaling pathway may be the main signaling pathways. CONCLUSION: The Shuangling extract could inhibit the inflammatory response induced by UC and regulate intestinal immune function through multiple targets and multiple channels, which provided a new option and theoretical basis for anti-UC.

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