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Integrated Network Pharmacology Analysis to Dissect the Protective Effect and Mechanism of Ruangan Xiaoji Decoction against Liver Fibrosis in Rat

作者
H. F. Xu,W. R. Zhu,T. W. Zhao
出处
期刊:Indian Journal of Pharmaceutical Sciences [Medknow]
卷期号:84 (S1)
标识
DOI:10.36468/pharmaceutical-sciences.spl.405
摘要

Ruangan Xiaoji decoction is a traditional Chinese medicine formula used clinically to treat liver fibrosis. However, due to the complex composition of Ruangan Xiaoji decoction, its potential anti-liver fibrosis and the combination mechanism remain unclear. The present work was to further investigate the active mechanism of Ruangan Xiaoji decoction against liver fibrosis using an integrated strategy of network pharmacology. In this study, network pharmacology analysis was performed to identify the active compounds and target genes, which might be responsible for the effect of Ruangan Xiaoji decoction. Meanwhile, the combined effect of Ruangan Xiaoji decoction on carbon tetrachloride-induced liver fibrosis rats and changes of biochemical and histopathology was detected. The results of the network pharmacology analysis showed 160 compounds and 337 potential target genes related to the treatment of Ruangan Xiaoji decoction with liver fibrosis. Functional enrichment analysis indicated that the potential mechanism was mainly associated with the Hepatitis B and phosphatidylinositol 3-kinase-protein kinase B signaling pathway. In addition, the carbon tetrachlorideinduced liver fibrosis rat was used to study the mechanism of Ruangan Xiaoji decoction against liver fibrosis. Compared with the model group, Ruangan Xiaoji decoction can alleviate the pathological damage and fibrosis of rat liver tissue, significantly reduce rat serum alanine aminotransferase, aspartate aminotransferase levels and significantly affect liver superoxide dismutase and malondialdehyde levels, and can significantly inhibit tumour necrosis factor alpha, interleukin 1 beta and interleukin 11 level. Western blot analysis showed that Ruangan Xiaoji decoction can down-regulate the expression of phosphorylated-p38 mitogen-activated protein kinase, phosphorylated phosphoinositide 3-kinase and phosphorylated protein kinase B protein.

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