Department of Rheumatology, Nanjing University of Chinese Medicine, Nanjing, China.
Department of Pneumology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.
Ann Med. 2022 Dec;54(1):541-552. doi: 10.1080/07853890.2022.2034931.
Interstitial lung disease (ILD) is associated with substantial morbidity and mortality, which is one of the key systematic manifestations of connective tissue disease (CTD). Tripterygium wilfordii, known as Leigongteng in Chinese, has been applied to treat connective tissue disease-related interstitial lung disease (CTD-ILD) for many years. Triptolide is a key effective component from Tripterygium wilfordii. But the molecular mechanism of Triptolide for treating CTD-ILD is not yet clear.
Gaining insight into the molecular mechanism of Triptolide intervention CTD-ILD, we used the method of network pharmacology. And then we conducted drug-target networks to analyse the potential protein targets between Triptolide and CTD-ILD. Finally, AutoDock Vina was selected for molecular docking.
By analysing the interaction genes between Triptolide and CTD-ILD, 242 genes were obtained. The top 10 targets of the highest enrichment scores were STAT3, AKT1, MAPK1, IL6, TP53, MAPK3, RELA, TNF, JUN, JAK2. GO and KEGG enrichment analysis exhibited that multiple signalling pathways were involved. PI3K-Akt, multiple virus infections, cancer signalling, chemokine, and apoptosis signalling pathway are the main pathways for Triptolide intervention CTD-ILD. And it is related to various biological processes such as inflammation, infection, cell apoptosis, and cancer. Molecular docking shows Triptolide can bind with its target protein in a good bond by intermolecular force.
This study preliminarily reveals the internal molecular mechanism of Triptolide interfere with CTD-ILD through multiple targets, multiple access, validated through molecular docking.KEY MESSAGESTriptolide intervention CTD-ILD, which are related to various biological processes such as inflammation, infection, cell apoptosis, and cancer.PI3K-Akt, multiple virus infections, and apoptosis signalling pathway are the main pathways for Triptolide intervention CTD-ILD.Triptolide can bind with related target protein in a good bond by Intermolecular force, exhibiting a good docking activity.
间质性肺病(ILD)与大量发病率和死亡率相关,是结缔组织疾病(CTD)的关键系统表现之一。雷公藤,在中国被称为雷公藤,多年来一直用于治疗与结缔组织疾病相关的间质性肺病(CTD-ILD)。雷公藤内酯醇是雷公藤的关键有效成分。但是,雷公藤内酯醇治疗 CTD-ILD 的分子机制尚不清楚。
为了深入了解雷公藤内酯醇干预 CTD-ILD 的分子机制,我们使用了网络药理学的方法。然后,我们进行了药物-靶标网络分析,以分析雷公藤内酯醇与 CTD-ILD 之间的潜在蛋白靶标。最后,选择 AutoDock Vina 进行分子对接。
通过分析雷公藤内酯醇与 CTD-ILD 之间的相互作用基因,得到了 242 个基因。富集得分最高的前 10 个靶标是 STAT3、AKT1、MAPK1、IL6、TP53、MAPK3、RELA、TNF、JUN、JAK2。GO 和 KEGG 富集分析表明,涉及多个信号通路。PI3K-Akt、多种病毒感染、癌症信号、趋化因子和细胞凋亡信号通路是雷公藤内酯醇干预 CTD-ILD 的主要通路。并且与炎症、感染、细胞凋亡和癌症等各种生物过程有关。分子对接表明,雷公藤内酯醇可以通过分子间力与靶标蛋白形成良好的结合。
本研究通过多靶点、多途径初步揭示了雷公藤内酯醇通过多个靶点干扰 CTD-ILD 的内在分子机制,通过分子对接得到了验证。
雷公藤内酯醇干预 CTD-ILD,与炎症、感染、细胞凋亡和癌症等各种生物过程有关。PI3K-Akt、多种病毒感染和细胞凋亡信号通路是雷公藤内酯醇干预 CTD-ILD 的主要通路。雷公藤内酯醇可以通过分子间力与相关靶标蛋白形成良好的结合,表现出良好的对接活性。