1,25-Dihydroxy vitamin D3 inhibits LPS-mediated inflammatory responses in endometriosis

Qiyu Zhong, Zhuang Jin, Jianyu Ma, Zhouzhou Liao, Huiling Lai, Hui‐Ling Lai, Shuqin Chen
Annals of medicine · 2025 · vol. 57(1) , pp. 2523563 · doi:10.1080/07853890.2025.2523563 · PMID:40579858 · PMC12207774 · W4411757902
article OA: gold CC0 ⤵ 2 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

1,25-dihydroxy vitamin D3 inhibited endometriosis lesion growth and suppressed LPS-mediated inflammatory responses by stabilizing IκBα and activating the VDR.

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Abstract

BACKGROUND: Endometriosis, a chronic immune-mediated inflammatory disease, remains elusive in its pathogenesis. Given vitamin D (VD)'s pivotal role in modulating innate and adaptive immune responses, we sought to elucidate how VD modulates inflammatory responses in endometriosis. MATERIALS AND METHODS: We isolated primary human ectopic endometrial stromal cells (EESCs) from ectopic endometrium of ovarian endometrioma, alongside Ishikawa cells, and subjected them to treatment with lipopolysaccharide (LPS), a potent inducer of inflammation, alongside varying concentrations of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), the biologically active form of VD, and its analog TEI-9647 (25-dehydro-1α-hydroxyvitamin D3-26,23-lactone). RESULTS: Our results revealed that 1,25(OH)2D3 significantly reversed LPS-induced cell proliferation, migration, and inflammatory factor production in EESCs and Ishikawa cells, and induced apoptosis. Additionally, 1,25(OH)2D3 inhibited the expression and nuclear translocation of phosphorylated p65 in LPS-activated EESCs and Ishikawa cells. Furthermore, 1,25(OH)2D3 counteracted LPS-induced suppression of VD receptor (VDR)/IκBα and enhancement of Toll-like receptor 4 (TLR4)/pyrin domain (PYD)-containing protein 3 (NLRP3) activation, while the addition of TEI-9647 reversed VD's regulatory effects on the NF-κB pathway. In vivo experimental results showed that 1,25(OH)2D3 significantly inhibited lesion growth, suppressed NF-κB pathway activation, and corresponding inflammatory phenotypes in a rat model of endometriosis. CONCLUSIONS: Collectively, these results underscore the potential of 1,25(OH)2D3 as a therapeutic target for endometriosis via VDR-dependent endometrial homeostasis regulation, suppressing LPS-mediated inflammatory responses and NF-κB signaling pathway through VDR activation and IκBα stabilization.

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Condition tags

endometriosis

MeSH descriptors

Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol Calcitriol

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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