Network pharmacology based investigation into the bioactive compounds and molecular mechanisms of Schisandrae Chinensis Fructus against drug-induced liver injury

肝损伤 化学 药理学 药品 生物化学 丙二醛 谷胱甘肽 中医药 超氧化物歧化酶 氧化应激 医学 替代医学 病理
作者
Xiankuan Li,Huijuan Yang,Jiongchang Xiao,Jian Zhang,Juan Zhang,Mei Liu,Yanchao Zheng,Lin Ma
出处
期刊:Bioorganic Chemistry [Elsevier BV]
卷期号:96: 103553-103553 被引量:28
标识
DOI:10.1016/j.bioorg.2019.103553
摘要

To investigate the against Drug-induced liver injury ingredients and their functional mechanisms in S. Chinensis Fructus. Liquid chromatograph-mass spectrometry analysis was performed on S. Chinensis Fructus extrac. The “Components-Target-Disease” network model was constructed by network pharmacology-based approaches. String analysis was performed to reveal enrichment of these target proteins, protein-protein interactions, pathways and related diseases. And experiment of APAP-induced drug-induced liver injury was to be verified. Cytoscape was used to determine the potential protein targets for these components in S. Chinensis Fructus, indicating that 17 against Drug-induced liver injury compounds in S. Chinensis Fructus regulate 52 diabetes-related proteins in 15 signal pathways and involve 14 core key targets. Verification experiment results that S. Chinensis Fructus prevented the elevation of serum biochemical parameters including aspartate aminotransferase (AST), alanine aminotransferase (ALT), purine nucleoside phosphorylase (PNP) and alkaline phosphatase (ALP) against acute liver failure. Additionally, S. Chinensis Fructus reduced the content of malondialdehyde (MDA), increased the levels of the Superoxide dismutase (SOD) and Glutathione (GSH), and inhibited the production of proinflammatory cytokines in APAP-induced hepatotoxicity. The mechanisms of S. Chinensis Fructus against Drug-induced liver injury were involved in the regulation of multiple targets, especially affecting the ErbB signaling pathways. The active ingredients of S. Chinensis Fructus may play a role against Drug-induced liver injury by participating in the regulation of inflammatory factors, oxidative stress.

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