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[1]吳鎧悅,張麗允,馮文敏,等.基于網絡藥理學探討西黃丸治療肝癌的作用機制[J].福建醫(yī)藥雜志,2024,46(02):118-122.[doi:10.20148/j.fmj.2024.02.032]
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基于網絡藥理學探討西黃丸治療肝癌的作用機制()
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《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
46
期數:
2024年02期
頁碼:
118-122
欄目:
基礎研究
出版日期:
2024-04-15

文章信息/Info

文章編號:
1002-2600(2024)02-0118-05
作者:
吳鎧悅張麗允馮文敏黃月萍劉亞茹朱亞玲
華僑大學醫(yī)學院,泉州 362021
關鍵詞:
西黃丸 肝癌 網絡藥理學 分子對接
分類號:
R285.5; R735.7
DOI:
10.20148/j.fmj.2024.02.032
文獻標志碼:
B
摘要:
目的 運用網絡藥理學和分子對接技術探討西黃丸治療肝癌的潛在作用機制。方法 利用TCMSP、化學專業(yè)數據庫及SwissTargetPrediction數據庫獲取西黃丸的活性成分及靶點; 從GeneCards、NCBI、DisGeNET及CTD數據庫收集肝癌相關靶點,并與活性成分靶點取交集; 采用STRING平臺和Cytoscape軟件構建靶點相互作用網絡,并借助DAVID數據庫進行GO和KEGG富集分析; 利用CB-Dock分子對接工具將活性成分與關鍵靶點進行分子對接。結果 共篩選出205個活性成分和324個與肝癌治療相關的潛在靶點,其中包括AR、CYP19A1、ESR1等61個關鍵靶點; GO和KEGG富集分析發(fā)現(xiàn)關鍵靶點參與凋亡過程的負調控、蛋白質磷酸化、細胞增殖的正調控等生物過程,調控HIF-1信號通路、PI3K-Akt信號通路、TNF信號通路等114條信號通路。分子對接結果顯示沒藥甾醇I、洋椿苦素、白藜蘆醇等活性成分與關鍵靶點之間均有較強的結合力。結論 西黃丸通過多成分、多靶點、多通路調控肝癌細胞的增殖、侵襲、遷移與凋亡,從而抑制肝癌的發(fā)生和發(fā)展。

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備注/Memo

備注/Memo:
通信作者:朱亞玲,Email:[email protected]
更新日期/Last Update: 2024-04-15