目的 通過網(wǎng)絡(luò)藥理學(xué)方法及分子對接探討雷公藤有效成分治療白塞病作用機(jī)制。方法 應(yīng)用中藥系統(tǒng)藥理學(xué)分析平臺（TCMSP）獲取雷公藤活性成分；利用PubChem和SwissTargetPrediction數(shù)據(jù)庫將活性成分轉(zhuǎn)化為基因名；通過Disgenet、GeneCards數(shù)據(jù)庫獲取白塞病的疾病靶點(diǎn)；利用Venny 2.1軟件繪制雷公藤主要成分基因與白塞病基因的共同靶點(diǎn)韋恩圖；應(yīng)用Cytoscape3.2.1軟件構(gòu)建“雷公藤–主要成分–白塞病”交集基因網(wǎng)絡(luò)圖；利用STRING數(shù)據(jù)庫對其作用靶點(diǎn)構(gòu)建蛋白相互作用（PPI）網(wǎng)絡(luò)分析；通過DAVID數(shù)據(jù)庫和微生信軟件進(jìn)行基因本體（GO）、京都基因與基因組百科全書（KEGG）富集分析，篩選出潛在通路并分析其作用機(jī)制，并利用分子對接技術(shù)驗(yàn)證。結(jié)果 從雷公藤中共獲得59個(gè)生物活性成分，對應(yīng)的作用靶點(diǎn)561個(gè)；白塞病疾病基因984個(gè)；通過篩選雷公藤作用于白塞病的共同靶點(diǎn)，得到73個(gè)交集基因；其核心靶點(diǎn)為腫瘤壞死因子（TNF）、蛋白激酶B1（Akt1）、基質(zhì)金屬蛋白酶9（MMP9）、信號傳導(dǎo)和轉(zhuǎn)錄激活蛋白3（STAT3）；核心通路為脂質(zhì)和動脈粥樣硬化信號通路、乙型肝炎信號通路、Th17細(xì)胞分化信號通路、癌癥信號通路、人巨細(xì)胞病毒感染信號通路等。分子對接技術(shù)顯示，去甲黑蔓酮酯與TNF、Akt1靶蛋白的結(jié)合能力較強(qiáng)，雷公藤三萜酸A與Akt1靶蛋白的結(jié)合能力較強(qiáng)。結(jié)論 雷公藤通過多靶點(diǎn)、多途徑發(fā)揮其整體調(diào)節(jié)效應(yīng)而治療白塞病。

Objective To explore the mechanism of active components of T. wilfordii in treatment of Behcet disease by network pharmacology. Methods The active components of T. wilfordii were obtained by TCMSP. The main components of T. wilfordii were transformed into the gene names by using PubChem and SwissTargetPrediction database. The targets of Behcet disease were obtained from Disgenet and GeneCards database. Venny 2.1 software was used to map the common target of the genes of the main components of T. wilfordii and Behcet disease. Cytoscape3.2.1 software was used to construct the intersection gene network diagram of “T. wilfordii–main component–Behcet disease”. The protein interaction network analysis (PPI) of the target was constructed by using STRING database. GO analysis and KEGG pathway enrichment analysis were conducted through DAVID database and Weisheng software to screen out potential pathways and analyze their mechanism of action. The molecular docking was used for validation. Results A total of 59 bioactive components were obtained from T. wilfordii, corresponding to 561 targets. 984 genes of Behcet disease. By screening the common targets of T. wilfordii on Behcet disease, 73 intersection genes were obtained. Its core targets may be TNF, Akt1, MMP9, and STAT3. The core pathways may be lipid and atherosclerosis signaling pathway, hepatitis B signaling pathway, Th17 cell differentiation signaling pathway, cancer signaling pathway, human cytomegalovirus infection signaling pathway, etc. Molecular docking shows that demethylregelin have good binding conformations with the core target of TNF and Akt1, triptotriterpenic acid A have good binding conformations with the core target of Akt1. Conclusion T. wilfordii can exert its global regulatory effect in treatment of Behcet disease through multi target and multi pathway.

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