ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2026
[Scutellarin improves metabolic dysfunction-associated steatotic liver disease in rats by regulating MMP7 and LCN2].
Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesTo identify the therapeutic targets and signaling pathways that mediate the therapeutic effect of scutellarin against metabolic dysfunction-associated steatotic liver disease (MASLD).
methodsThe differentially expressed genes (DEGs) in liver tissues of MASLD patients and healthy individuals were obtained from the GSE89632 dataset. The potential targets of scutellarin were screened using the PharmMapper database, and a drug-target network was constructed using Cytoscape. Functional enrichment analysis was performed using GO and KEGG pathway analysis. The intersection of scutellarin's target genes and the DEGs formed the potential therapeutic (PT) genes. Protein-protein interaction (PPI) networks were constructed using STRING to identify the key therapeutic (KT) genes. Molecular docking and dynamics simulations were used to assess the drug-target relationship. In a rat model of MASLD treated with different doses of scutellarin, the changes in serum biochemical parameters and liver pathology were analyzed.
resultsA total of 810 DEGs and 12 PT genes were identified, and GO and KEGG analyses suggested their involvement in inflammation regulation, cytokine response, fibrosis, and metabolism. In the rat models of MASLD, treatment with scutellarin significantly improved insulin resistance, liver function, lipid levels, inflammation, and hepatic pathology in a dose-dependent manner, and high-dose scutellarin produced better therapeutic effects than simvastatin. Scutellarin treatment significantly upregulated MMP7 and downregulated LCN2 expression in the mouse livers.
conclusionsScutellarin ameliorates MASLD in rats possibly by modulating hepatic MMP7 and LCN2 expressions.
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