ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2025
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Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2025. 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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4 authors.
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Abstract
objectivesTo explore therapeutic mechanism of
methodsNetwork pharmacology analysis was used to predict the active components of HGT against NAFLD and their potential targets, and the core targets were identified using the protein-protein interaction network, followed by GO and KEGG pathway enrichment analyses. A rat model of high-fat diet (HFD)-induced NAFLD was used to test the effects of saline, silymarin, and low-, moderate-, and high-dose HGT on serum levels of ALT, AST, LDL, LDH, TG and TC, liver histopathology, and protein and mRNA expressions of ACC1, FASN, AMPK and m-TOR. In free fatty acid (FFA)-induced HepG2 cells, the effects of blank and HGT-medicated sera, compound C (an AMPK inhibitor), and MHY1485 (a mTOR agonist) were tested on cell viability, intracellular lipid deposition, TC and TG levels, and expressions of ACC1, FASN, AMPK and m-TOR.
resultsWe identified 130 active components in HGT, 267 common targets with NAFLD, and 53 core gene nodes, nearly half of which were involved in lipid metabolism. HGT treatment of NAFLD was closely associated with lipid and atherosclerosis signaling, insulin resistance signaling, and AMPK signaling. In rat models of NAFLD, HGT significantly alleviated liver injury and lipid accumulation, and suppressed mRNA and protein expressions of ACC1 and FASN. In FFA-induced HepG2 cells, HGT-medicated serum obviously reduced TG and TC levels and inhibited ACC1 and FASN mRNA and protein expressions. The results of
conclusionsHGT alleviates NAFLD in rats by activating the AMPK/m-TOR signaling pathway and reducing lipid synthesis.
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