ArticlePharmaceutical biology2026
Multi-target protective effects of
Article in Pharmaceutical biology, 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
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study integrated Therapeutic efficacy was evaluated using a MASH mouse model, AML12 hepatocytes, and RAW264.7 macrophages. Active constituents were identified by UHPLC-HRMS, and potential targets were predicted via SwissTargetPrediction and GEO databases, followed by PPI network construction, GO/KEGG enrichment analysis, molecular docking, and molecular dynamics simulation. AP markedly reduced body weight, liver index, and serum AST, ALT, TG, TC, and LDL-c levels, and attenuated hepatic steatosis, inflammation, and fibrosis. In AML12 cells, AP suppressed lipogenesis by downregulating SREBP-1c, FASN, and SCD1, while promoting fatty acid β-oxidation through CPT1A upregulation. In RAW264.7 macrophages, AP inhibited LPS-induced expression of TNF-α, IL-1β, and IL-6. A total of 83 active constituents and 25 key targets were identified, with HMGCR and AXL emerging as hub nodes. Agrimol B (AGB) exhibited favorable binding affinity and structural stability toward both targets. Mechanistically, AGB inhibited HMGCR, reduced SREBP-2 nuclear translocation, and enhanced LXRα/β-mediated cholesterol efflux, maintaining hepatic cholesterol homeostasis. These findings demonstrate that AP ameliorates MASH through coordinated regulation of lipid metabolism, inflammatory suppression, and collagen deposition, with AGB representing a promising bioactive candidate warranting further investigation.
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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.