ArticleJournal of immunology research2026
Therapeutic Potential of Thiosemicarbazone Derivative in LPS-Induced Mastitis: Dual Modulation of Inflammatory Response and Blood-Milk Barrier Integrity.
Article in Journal of immunology 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.
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Abstract
Mastitis is a prevalent inflammatory disorder in women, this condition exhibits a particularly elevated prevalence among breastfeeding women, which significantly compromises mammary health and lactation function. This research explored the anti-inflammatory properties of YWJ-6 in lipopolysaccharide (LPS)-induced mastitis, its protective role on the blood-milk barrier (BMB), and the underlying mechanisms. An LPS-induced mastitis rat model was established. H&E staining assessed mammary tissue damage, and myeloperoxidase (MPO) activity was measured. RT-qPCR and IHC were used to demonstrate interleukin 1β (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNFα) expression. These data indicated that inflammatory injury was alleviated. Following drug treatment, MPO expression and the mRNA/protein expression of these inflammatory factors were suppressed. Immunofluorescence staining analyzed the distribution of Zonula Occludens-1 (ZO-1), Occludin, and Claudin-3. WB quantitatively detected ZO-1 and Occludin expression, confirming that YWJ-6 promoted tight junction (TJ) protein expression restoration and distribution integrity, repairing the damaged BMB. Consistently, Evans blue extravasation assay demonstrated that YWJ-6 reduced mammary vascular permeability, providing direct functional evidence for BMB protection. mIHC detected the colocalization of CD68, MPO, and nuclear factor-kappa B (NF-κB) p65 subunit (NF-κB p65), showing that YWJ-6 modulated inflammatory cell infiltration and p65 activation. RT-qPCR, WB, and ELISA assays in HC11 and RAW264.7 cells confirmed that YWJ-6 downregulated inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and IL-1β, IL-6 and TNF-α expression in HC11 cells, and suppressed agent responsible for inflammation secretion in RAW264.7 cells. WB and immunofluorescence showed that YWJ-6 inhibited inhibitor of NF-κB alpha (IκBα) and NF-κB p65 phosphorylation in both HC11 and RAW264.7 cells. In conclusion, YWJ-6 exerts dual protective effects by targeting NF-κB signaling pathway activation, providing experimental evidence for mastitis treatment in future.
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