Abstract
Objective To use network pharmacology and molecular docking technology in predicting the main active ingredients and targets of Qushi Huayu Decoction (QHD) treatment in Nonalcoholic Fatty Liver Disease (NAFLD) and explore the potential mechanisms of its multi-component-multi-target-multi-pathway. Materials and Methods The main chemical components of QHD were searched using traditional Chinese medicine system pharmacology technology platform (TCMSP) and PubChem database. The main chemical components of the prescription were ADMET screened by the ACD/Labs software. The main active ingredient was screened by 60% oral bioavailability, and 60% of “bad” ingredients were removed from the drug-like group. Swiss Target Prediction, the SEA, and HitPick systems were sequentially used to search for the target of each active ingredient, and a network map of the QHD's target of the active ingredient was constructed. Genome annotation database platforms (GeneCards, OMIM, and DisGeNET) were used to predict action targets related to fatty liver disease. “Drug-Disease-Target” network diagram could be visualized with the help of Cytoscape (3.7.1) software. UniProt and STRING database platforms were used to build a protein interaction network. The KEGG signal pathway and DAVID platform were analyzed for biological process enrichment. Results A total of 128 active ingredients and 275 corresponding targets in QHD were discovered through screening. 55 key target targets and 27 important signaling pathways were screened, such as the cancer pathway, P13K-AKT signaling pathway, PPAR signaling pathway, and other related signaling pathways. Conclusions The present study revealed the material basis of QHD and discussed the pharmacological mechanism of QHD in fatty liver, thus providing a scientific basis for the clinical application and experimental research of QHD in the future.
Highlights
Over recent years, the incidence of fatty liver has been increasing, especially among the younger population [1]
Nonalcoholic Fatty Liver Disease (NAFLD) belongs to the category of “accumulation,” “fat qi,” “ruffian full,” and “hypochondriac pain” in Traditional Chinese medicine (TCM) [16], which has a deep understanding of the etiology, pathogenesis, syndrome differentiation, and drug selection of NAFLD, while the mechanism and pathway of Chinese medicine treatment remain unclear [17]
We found that liver biliverdin reductase A (BVRA) inhibits the protective effect of glycogen synthase kinase 3 (GSK3β) on hepatic steatosis by enhancing serine 9 phosphorylation
Summary
The incidence of fatty liver has been increasing, especially among the younger population [1]. Fatty liver disease is pathologically characterized by hepatocyte steatosis and fat accumulation caused by different factors. It can be divided into alcoholic fatty liver and Nonalcoholic Fatty Liver Disease (NAFLD) [2]. NAFLD refers to the clinical-pathological syndrome of hepatic steatosis caused by excessive deposition of triglyceride- (TG-) based lipids in hepatocytes, excluding excessive drinking history and obvious risk factors for liver damage. The pathogenesis of NAFLD has not been fully elucidated and is currently believed to be related to genetics, associated diseases, lifestyle, environment, and other multiple gene factors [3]. NAFLD is considered a more extensive liver manifestation of potential
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