Celecoxib, a selective COX‑2 inhibitor, markedly reduced the severity of tamoxifen‑induced adenomyosis in a murine model

Zhixing Jin, Xiaoyi Wu, Haiou Liu, Congjian Xu
Experimental and therapeutic medicine · 2020 · vol. 19(5) , pp. 3289–3299 · doi:10.3892/etm.2020.8580 · PMID:32266025 · W3010507200
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Celecoxib, a COX-2 inhibitor, reduced tamoxifen-induced adenomyosis severity in mice by suppressing estrogen, reversing EMT, and relieving fibrosis.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

The paper evaluated whether the selective COX-2 inhibitor celecoxib can reduce development and severity of tamoxifen-induced adenomyosis in neonatal ICR mice, using 60 days of oral treatment after tamoxifen exposure. Lesion formation and myometrial infiltration were quantified histologically, while pain-related behavior was assessed with repeated hotplate thermal latency testing, and epithelial–mesenchymal transition, COX-2, aromatase P450, CD31, E-cadherin/N-cadherin expression, uterine estrogen levels (ELISA), and fibrosis (Masson trichrome) were measured. Celecoxib significantly decreased the depth of myometrial infiltration, increased thermal response latency at higher doses, upregulated E-cadherin and downregulated N-cadherin, reduced fibrosis, and lowered uterine estrogen and aromatase P450 expression; the authors frame these results as consistent with reduced estrogen production, reversal of EMT, and less fibrosis. The study’s main limitation is that it is confined to a murine tamoxifen-induced model without demonstration of effects in human adenomyosis. This paper is centrally about endometriosis and/or adenomyosis — specifically adenomyosis, testing celecoxib’s impact on tamoxifen-induced adenomyosis severity and related mechanisms.

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Abstract

The aim of the present study was to evaluate the effects of the selective cyclooxygenase (COX)-2 inhibitor celecoxib on the development of uterine adenomyosis in mice. ICR neonatal mice were first exposed to tamoxifen to establish a mouse model of adenomyosis. Following 60 days of celecoxib treatment, pathological formation of adenomyosis lesions and the depth of myometrial infiltration were evaluated using hematoxylin and eosin staining. To examine thermal pain modulation in mice, a hotplate test was conducted every 15 days from postnatal day 30 onwards. Immunohistochemistry was performed to assess the expression of aromatase P450, N-cadherin, E-cadherin, COX-2 and cluster of differentiation 31, whereas the levels of estrogen were analyzed in uterine tissue homogenates using ELISA. Masson trichrome staining was performed to assess the extent of fibrosis in the uterus. Celecoxib treatment significantly inhibited the depth of infiltration into the myometrium, resulting in significantly reduced disease severity. Treatment with high doses of celecoxib significantly prolonged thermal response latency. Following celecoxib treatment, the expression of E-cadherin was significantly increased whereas the expression of N-cadherin was significantly decreased. Concomitantly, the extent of fibrosis was also reduced following celecoxib treatment. Uterine tissue homogenates isolated from mice treated with both high and low doses of celecoxib exhibited lower concentrations of estrogen and decreased expression of aromatase P450. These observations suggest that celecoxib reduces adenomyosis severity by suppressing estrogen production in the uterus, reversing epithelial-mesenchymal transition and relieving fibrosis. Taken together, the results of the present study support the potential use of celecoxib, a selective COX-2 inhibitor, for the treatment of adenomyosis.

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adenomyosis

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