基于网络药理学和分子对接探讨墨旱莲治疗肝损伤作用机制研究

To Explore the Mechanism of the Treatment of Liver Injury by Ecliptae Herba Based on Network Pharmacology and Molecular Docking

摘要: 目的：墨旱莲是临床上的常用中药之一且应用广泛。研究表明，墨旱莲具有治疗肝损伤的功效，但其作用机制尚不明确。我们应用基于网络药理学的方法及分子对接来系统地揭示墨旱莲对治疗肝损伤的潜在机制。方法：通过TCMSP检索筛选墨旱莲的活性成分及靶点，在GeneCards数据库中寻找肝损伤的相关靶点，取交集基因进行蛋白互作分析，GO生物富集及Kegg富集分析，最后采用分子对接进行验证。结果：得到墨旱莲的活性成分有10个，得到交集基因133个，蛋白互作分析发现TP53、AKT1和MAPK1治疗肝损伤的作用，Kegg富集结果发现，旱莲治疗肝损伤主要通过Hepatitis B、Pathways in cancer、Bladder cancer、TNF signaling pathway等信号通路进行调控。分子对接结果显示，墨旱莲中的活性成分Linarin、quercetin、Pratensein等成分与TP53、AKT1和 MAPK1具有较好的结合能力。结论：墨旱莲可能是通过Linarin、quercetin、Pratensein等化学成分调控Hepatitis B、Pathways in cancer、Bladder cancer等信号通路上的TP53、AKT1和 MAPK1等基因发挥治疗肝损伤的作用。

Abstract: Objective: Ecliptae Herba is one of the commonly used traditional Chinese medicine in clinic and is widely used. Studies have shown that Ecliptae Herba has the effect of treating liver injury, but its mechanism is not clear. We systematically revealed the potential mechanism of Ecliptae Herba on the treatment of liver injury by using network pharmacological methods and molecular pairs. Methods: The active components and targets of Ecliptae Herba were screened by TCMSP retrieval, and the related targets of liver injury were found in genecards database. The intersection genes were taken for protein interaction analysis. It was found that GO bioaccumulation and KEGG enrichment were analyzed. Finally, molecular docking was used for verification. Results: There were 10 active components and 133 intersection genes. Protein interaction analysis showed that TP53, AKT1 and mapk1 could treat liver injury. KEGG enrichment showed that the treatment of liver injury was mainly regulated by hepatitis B, pathways in cancer, bladder cancer, TNF signaling pathway and other signal pathways. The results of molecular docking showed that the active components linarin, quercetin and pratensein in Ecliptae Herba had good binding ability with TP53, AKT1 and mapk1. Conclusion: Ecliptae Herba may play a role in the treatment of liver injury by regulating TP53, AKT1 and mapk1 genes on hepatitis B, pathways in cancer and bladder cancer through linarin, quercetin and pratensein.