Frontiers in pharmacology · 2026
Microplastic exposure is associated with enhanced PI3K-Akt signaling in DSS-induced colitis: integrated bioinformatics analyses and in vivo validation.
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Lu Lisha, Yang Yuanming, He Shunyong, Huang Shaogang, Li Yulong
Аннотация
BACKGROUND: Microplastics (MPs) are widely distributed in the environment and may aggravate ulcerative colitis (UC), but the underlying molecular mechanisms remain unclear.
METHODS: We integrated network toxicology, RNA-seq-based differential expression analysis, molecular docking, GeneMANIA-based functional association analysis, and experimental validation in a murine DSS-induced colitis model.
RESULTS: We identified 421 MP-related and 6,452 UC-related targets, including 265 overlapping targets. PIK3CD, PIK3CA, SRC, PTPN11, and EGFR were prioritized as hub targets with stable ligand binding. Enrichment analyses implicated the PI3K-Akt, JAK-STAT, T-cell receptor, and HIF-1 signaling pathways. In vivo experiments showed that MP exposure increased the colonic abundance of these five proteins and enhanced p-PI3K and p-AKT signals in DSS-induced colitis.
CONCLUSION: MP exposure is associated with enhanced PI3K-Akt signaling in experimental colitis. These findings provide preliminary biological support for the PI3K-Akt pathway as a potentially relevant mechanism linking MP exposure to UC aggravation.
METHODS: We integrated network toxicology, RNA-seq-based differential expression analysis, molecular docking, GeneMANIA-based functional association analysis, and experimental validation in a murine DSS-induced colitis model.
RESULTS: We identified 421 MP-related and 6,452 UC-related targets, including 265 overlapping targets. PIK3CD, PIK3CA, SRC, PTPN11, and EGFR were prioritized as hub targets with stable ligand binding. Enrichment analyses implicated the PI3K-Akt, JAK-STAT, T-cell receptor, and HIF-1 signaling pathways. In vivo experiments showed that MP exposure increased the colonic abundance of these five proteins and enhanced p-PI3K and p-AKT signals in DSS-induced colitis.
CONCLUSION: MP exposure is associated with enhanced PI3K-Akt signaling in experimental colitis. These findings provide preliminary biological support for the PI3K-Akt pathway as a potentially relevant mechanism linking MP exposure to UC aggravation.