Heat-inactivated Bifidobacterium adolescentis LA20 alleviates doxorubicin-induced senescence and barrier dysfunction in feline intestinal epithelial cells.
AI interpretation is pending for this paper.
Open original publication →What the AI sees
Not AI summarized yet.
Research significance
Pending deeper interpretation.
Source abstract
OBJECTIVE: To investigate the protective effects and molecular mechanisms of heat-inactivated Bifidobacterium adolescentis LA-20 (HT-LA20) against doxorubicin (DOX)-induced senescent injury in feline intestinal epithelial cells (FIECs). METHODS: This in vitro experimental study was conducted from November 1, 2025, through August 31, 2026, and involved only FIECs. No clinical patients or animals were included. The DOX-induced injury and senescence model was established in FIECs. The effects of HT-LA20 on cellular senescence and related proteins were evaluated by senescence-associated β-galactosidase staining, cell viability assays, and ELISA. Transcriptomic sequencing and untargeted metabolomics were integrated to elucidate the molecular regulatory mechanisms. RESULTS: Cell-based assays and transcriptomic and untargeted metabolomic analyses were performed with 4 independent biological replicates/group. HT-LA20 reversed DOX-induced reductions in cell viability and cellular senescence; upregulated tight junction proteins and mucins 1 and 2; suppressed release of IL-1β, tumor necrosis factor-α, IL-8, monocyte chemoattractant protein 1, and matrix metalloproteinase 1; and promoted VEGF and basic fibroblast growth factor (bFGF) secretion. Transcriptomic and metabolomic analyses showed that HT-LA20 reversed DOX-induced omic disturbances. Integrated multiomics Kyoto Encyclopedia of Genes and Genomes enrichment analysis indicated that its effects centered on the retinol metabolism-serotonergic synapse-intestinal immunoglobulin A immune network multitarget axis and regulation of inflammatory pathways, including nuclear factor κ B and Toll-like receptor signaling. CONCLUSIONS: HT-LA20 effectively alleviates DOX-induced injury in FIECs by restoring intestinal epithelial barrier function and suppressing inflammatory senescence. CLINICAL RELEVANCE: These findings provide a theoretical basis for subsequent in vivo studies on postbiotics for chemotherapy-induced intestinal injury in veterinary medicine; clinical application requires further validation.