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.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.