Lv Shujing, Yu Honghong, Liu Xinyue, Gao Xiaoyan
School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Front Pharmacol. 2021 Jun 28;12:683707. doi: 10.3389/fphar.2021.683707. eCollection 2021.
Atorvastatin is a widely used lipid-lowering drug in the clinic. Research shows that taking long-term atorvastatin has the risk of drug-induced liver injury (DILI) in most patients. Hugan tablets, a commonly used drug for liver disease, can effectively lower transaminase and protect the liver. However, the underlying mechanism of Hugan tablets alleviating atorvastatin-induced DILI remains unclear. To address this problem, comprehensive chemical profiling and network pharmacology methods were used in the study. First, the strategy of "compound-single herb-TCM prescription" was applied to characterize the ingredients of Hugan tablets. Then, active ingredients and potential targets of Hugan tablets in DILI treatment were screened using network pharmacology, molecular docking, and literature research. In the end, the mechanism of Hugan tablets in treating atorvastatin-induced DILI was elucidated. The results showed that Hugan tablets can effectively alleviate DILI induced by atorvastatin in model rats, and 71 compounds were characterized from Hugan tablets. Based on these compounds, 271 potential targets for the treatment of DILI were predicted, and 10 key targets were chosen by characterizing protein-protein interactions. Then, 30 potential active ingredients were screened through the molecular docking with these 10 key targets, and their biological activity was explained based on literature research. Finally, the major 19 active ingredients of Hugan tablets were discovered. In addition, further enrichment analysis of 271 targets indicated that the PI3K-Akt, TNF, HIF-1, Rap1, and FoxO signaling pathways may be the primary pathways regulated by Hugan tablets in treating DILI. This study proved that Hugan tablets could alleviate atorvastatin-induced DILI through multiple components, targets, and pathways.
阿托伐他汀是临床上广泛使用的降脂药物。研究表明,大多数患者长期服用阿托伐他汀存在药物性肝损伤(DILI)风险。护肝片是一种常用的肝病治疗药物,能有效降低转氨酶并保护肝脏。然而,护肝片减轻阿托伐他汀所致DILI的潜在机制尚不清楚。为解决这一问题,本研究采用了综合化学表征和网络药理学方法。首先,应用“化合物-单味中药-中药复方”策略对护肝片成分进行表征。然后,通过网络药理学、分子对接和文献研究筛选出护肝片治疗DILI的活性成分和潜在靶点。最后,阐明了护肝片治疗阿托伐他汀所致DILI的机制。结果表明,护肝片能有效减轻模型大鼠阿托伐他汀所致的DILI,从护肝片中鉴定出71种化合物。基于这些化合物,预测了271个治疗DILI的潜在靶点,并通过蛋白质-蛋白质相互作用表征选择了10个关键靶点。然后,通过与这10个关键靶点的分子对接筛选出30种潜在活性成分,并基于文献研究解释了它们的生物学活性。最后,发现了护肝片的19种主要活性成分。此外,对271个靶点的进一步富集分析表明,PI3K-Akt、TNF、HIF-1、Rap1和FoxO信号通路可能是护肝片治疗DILI所调控的主要通路。本研究证明,护肝片可通过多种成分、靶点和通路减轻阿托伐他汀所致的DILI。