ArticleJournal of biochemical and molecular toxicology2026
Network Pharmacology-Based Prediction and In Vivo Validation of Fumonisin B1-Induced Liver Injury and Early Fibrosis.
Article in Journal of biochemical and molecular toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
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Who cites it
1 citing paper in PubMed.
- Network Pharmacology-Based Prediction and In Vivo Validation of Fumonisin B1-Induced Liver Injury and Early Fibrosis.Journal of biochemical and molecular toxicology · 2026Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Fumonisin B1 (FB1) is a widespread mycotoxin contaminating food and feed, exhibiting severe hepatotoxicity. This study aimed to systematically investigate the underlying molecular mechanisms of FB1-induced liver injury and early liver fibrosis by combining network pharmacology with an in vivo animal model. First, network pharmacology and molecular docking were utilized to screen the core targets and key signaling pathways of FB1-induced hepatotoxicity. Subsequently, an in vivo C57BL/6 mouse model was established via intragastric administration of FB1 (5 mg/kg/day for 28 days). Serum levels of liver function and fibrosis markers (ALT, AST, HA, LN, PCIII, CIV) were measured. Histopathological changes and collagen deposition in liver tissues were evaluated using HE and Masson's trichrome staining. The relative mRNA expression of inflammation- (TNF-α, IL-1β, IL-6) and fibrosis-related core genes (TGF-β1, α-SMA, COL1A1) was quantified by qPCR. Network pharmacology predicted that inflammatory responses and fibrosis-related pathways are central to FB1 hepatotoxicity. In vivo experiments confirmed that FB1 exposure significantly elevated serum ALT and AST levels, as well as the four indices of liver fibrosis (p < 0.001). Histopathology revealed severe hepatocyte necrosis, inflammatory cell infiltration, and massive deposition of blue-stained collagen fibers. Furthermore, qPCR results demonstrated that FB1 significantly upregulated the expression of pro-inflammatory cytokines, strongly activated the TGF-β1 signaling pathway, and promoted the high expression of the hepatic stellate cell (HSC) activation marker (α-SMA) and extracellular matrix (COL1A1). In conclusion, FB1 drives the pathogenesis of early liver fibrosis by inducing sustained hepatic inflammation and activating the TGF-β1 signaling pathway, which promotes HSC activation and excessive extracellular matrix deposition. This study provides a vital theoretical basis for elucidating the target-organ toxicity mechanisms of mycotoxins and identifying potential interventions.
Indexed as
Identifiers
42852606What 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.