[Role of mast cells in estrogen-mediated experimental endometriosis in rats].

Lin KQ, Kaiqing Lin, Kai-qing Lin, Zhu LB, Li-bo Zhu, Libo Zhu, Xinmei Zhang, Xin-mei Zhang, Zhang XM, Lin J, Jun Lin
Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2015 · vol. 44(3) , pp. 269–77 · doi:10.3785/j.issn.1008-9292.2015.05.06 · PMID:26350007 · PMC10396894 · W1409281050
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Estrogen promotes endometriotic lesion growth in rats by activating mast cells, potentially mediated by increased TNF-α and NGF.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 · read from full text ⓘ

The paper investigated the role of mast cells in estrogen-mediated experimental endometriosis in rats, using an animal model to assess how estrogen influences endometriosis-like lesions and whether mast cells contribute to those effects. It reports that mast cell involvement is linked to the estrogen-driven development or maintenance of endometriosis lesions. A major limitation is that the study is conducted in a rat experimental setting, which may not directly reproduce the cellular interactions and hormonal dynamics in human disease. This paper is centrally about endometriosis — it examines how mast cells participate in estrogen-mediated development of experimental endometriosis in rats.

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Abstract

OBJECTIVE: To investigate the role of mast cells in the pathogenesis of estrogen-mediated experimental endometriosis in rats. METHODS: Endometriosis model was established by transplanting autologous fragments of uterus to the inner surface of the abdominal wall in 24 un-pregnant female Sprague Dawley rats. The rats were divided randomly into three groups (n=8 in each group), and were injected with different doses of estrogen: high-dose group (200 μg·kg⁻¹·d⁻¹), low-dose group (100 μg·kg⁻¹·d⁻¹) and the control group (0 μg·kg⁻¹·d⁻¹). The ovaries were surgically removed in high-dose and low-dose groups. Four rats were sacrificed in each group at 2 and 4 weeks after surgery. Their serum estradiol levels, size of lesions, total number of mast cells and degranulations, serum TNF-α levels, expression of tryptase and NGF in tissues were analyzed and compared among groups. RESULTS: The mean levels of serum estradiol 2 weeks and 4 weeks after model established and serum TNF-α at 4 weeks in estrogen-treated groups were significantly higher than those in control group (all P<0.05). The mean size of endometriotic lesions in the estrogen-treated groups was also significantly larger than that in the control group 2 weeks and 4 weeks after model established (all P<0.05). Meanwhile, both at week 2 and week 4, the mean ratio of degranulation/total number of mast cells by toluidine blue staining in low-dose estrogen group was significantly higher than that in the control group (P<0.05). The expression of NGF in high-dose estrogen group was significantly higher than that in the control group at week 4(P<0.05). CONCLUSION: Estrogen can promote the growth of endometriotic lesions and may mediate the pathogenesis of endometriosis by activating mast cells, which may be associated with increasing TNF-α and NGF levels.
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Condition tags

endometriosis

MeSH descriptors

Endometriosis Estrogens Mast Cells Animals Cell Degranulation Disease Models, Animal Endometriosis Estrogens Female Mast Cells Nerve Growth Factor Nerve Growth Factor Pregnancy Rats Rats, Sprague-Dawley Tumor Necrosis Factor-alpha Tumor Necrosis Factor-alpha

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