ArticleJournal of inflammation research2026
Article in Journal of inflammation research, 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
Introduction: Non-alcoholic fatty liver disease (NAFLD) is a metabolic disorder characterized by lipid accumulation in hepatocytes. Our previous study demonstrated that the herbal pair (HS) of Astragalus Radix (HQ) and Dioscoreae Rhizoma (SY) reduces blood lipids and improves hepatic lipid metabolism in high-fat diet-fed mice. Purpose: This study aimed to investigate the effects and potential active ingredients of HS in treating NAFLD using Materials and Methods: Forty-eight male C57BL/6 mice (4 weeks old, 18-20 g) were fed a high-fat diet for 12 weeks to establish the NAFLD model (success rate: 87.5%). Successfully modeled mice were randomly divided into five groups (n=7 per group): NAFLD model (M), HS high-dose (HSH, approximately 18.9 g/kg/day), HS medium-dose (HSM, approximately 12.6 g/kg/day), HS low-dose (HSL, approximately 6.3 g/kg/day), and simvastatin (SV, 5 mg/kg), with a control group (C, n=8) receiving normal diet. After 4 weeks of treatment, efficacy was evaluated via oral glucose tolerance tests (OGTT), serum biochemical parameters (TC, TG, LDL, HDL, ALT, AST, CR, UA, BUN), and hematoxylin-eosin (H&E) staining. Urinary Results: HS treatment improved glucose tolerance, ameliorated serum biochemical abnormalities (TC, TG, LDL, ALT, AST), and reduced hepatic steatosis in NAFLD mice. Urinary metabolomics identified 43 metabolites, of which 17 were selected as differential metabolites (VIP > 1, P < 0.05), including glycine, threonine, citrate, pyruvate, carnitine, and 3-hydroxybutyrate. Ten metabolic pathways were significantly altered (P < 0.05), including the TCA cycle, glycolysis/gluconeogenesis, pyruvate metabolism, and glycine/serine/threonine metabolism. HPLC/LTQ-Orbitrap-MS analysis identified 8 potential active ingredients in HS: ononin, raffinose, erucamide, calycosin, sucrose, formononetin, arachidic acid, and adenosine. Molecular docking suggested that these ingredients may bind to 9 candidate targets (ADIPOQ, INS, TNF, LEP, PPARA, FGF21, CYP2E1, PNPLA3, SREBF1) with favorable binding energies. Conclusion: The combination of urinary metabolomics and molecular docking provides a feasible exploratory approach to identify potential active ingredients and metabolic pathways associated with the anti-NAFLD effects of HS. These findings suggest that HS may have potential therapeutic value for NAFLD.
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