ArticleScientific reports2019
Multiomics analysis profile acute liver injury module clusters to compare the therapeutic efficacy of bifendate and muaddil sapra.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 10 citations in OpenAlex.
- MALAT1 promotes acetaminophen-induced hepatocyte pyroptosis by stabilizing Rac1 through its interaction with MTDH and the hepatoprotective role of muniziqi saifula.Molecular and cellular biochemistry · 2026Article
- Proteomic profiles screening identified novel exosomal protein biomarkers for diagnosis of lung cancer.Clinical proteomics · 2025Article
- Molecular mechanism of geniposide against ANIT-induced intrahepatic cholestasis by integrative analysis of transcriptomics and metabolomics.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Integrative Analysis of Transcriptome and Metabolome to Illuminate the Protective Effects of Didymin against Acute Hepatic Injury.Mediators of inflammation · 2023Article
- Multi-omics integration reveals the hepatoprotective mechanisms of ursolic acid intake against chronic alcohol consumption.European journal of nutrition · 2022Article
- Effects ofMolecules (Basel, Switzerland) · 2019Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
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Abstract
The pathogenesis of acute liver injury has been plagued by biologists and physicians. We know little about its therapeutic mechanism. Therefore, this study explored the mechanism of bifendate and muaddil sapra in the treatment of acute liver injury. Firstly, co-expression and cluster analysis of disease-related genes were carried out, and the Go function and KEGG pathway of modules and related genes were identified. Secondly, pivot analysis of modules can identify key regulators. On the other hand, based on the acute liver injury induced by CCl4, we use the combined analysis of proteomics and transcriptome to find therapeutic targets and related mechanisms of drugs. A total of 21 dysfunction modules were obtained, which were significantly involved in immune system, hepatitis and other related functions and pathways. Transcriptome analysis showed 117 targets for bifendate treatment, while 119 for muaddil sapra. Through exploring the mechanism, we found that the two drugs could modulate the module genes. Moreover, bifendate regulate the dysfunction module through ncRNA (SNORD43 and RNU11). Muaddil sapra can mediate dysfunction modules not only by regulating ncRNA (PRIM2 and PIP5K1B), but also by regulating TF (STAT1 and IRF8), thus having a wider therapeutic potential. On the other hand, proteome analysis showed that bifendate mainly regulated Rac2, Fermt3 and Plg, while muaddil sapra mainly regulated Sqle and Stat1. In addition, muaddil sapra regulates less metabolic related proteins to make them more effective. Overall, this study not only provides basic theory for further study of the complex pathogenesis of acute liver injury, but also provides valuable reference for clinical use of bifendate and muaddil sapra in the treatment of acute liver injury.
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