[Role of estrogen, estrogen receptors, and aromatase in the pathogenesis of uterine adenomyosis].

OBJECTIVE: To study the role of estrogen (E2), estrogen receptor (ER) and aromatase (P450arom) in the pathogenesis of uterine adenomyosis. METHODS: Paraffin-embedded specimens of the uterine tissue from patients with uterine adenomyosis and patients with cervical lesions (CIN; control) were examined for expressions of E2, ER and P450arom by immunohistochemistry and ELISA. The cells isolated from the lesions of patients with adenomyosis were cultured in vitro, and the changes in cell growth in response to treatments with E2, ER inhibitor, ER inhibitor + E2, estrogen deprivation, and estrogen deprivation+ ICI182780 were assessed using CCK-8 method. RESULTS: The expression levels of E2, ER, and P450arom were significantly higher in adenomyosis ectopic lesions and eutopic endometrium than in the myometrium and endometrium in the control group (P<0.05); no significant difference in E2 and P450arom expressions was found between adenomyosis ectopic lesions and eutopic endometrium (P>0.05), while the expression levels of ER in ectopic lesions was significantly higher than that in eutopic endometrium. The cell inhibition rates were similar between ER inhibitor group and ER inhibitor + Estrogen activation group (P>0.05), and was significantly higher in estrogen deprivation+ ER inhibitor group than in estrogen deprivation group (P<0.05). CONCLUSION: The high expression levels of E2, ER, and P450arom in adenomyosis ectopic lesions and eutopic endometrium promote uterine adenomyosis cell proliferation, in which process E2 combines with ER to execute its biological effect; ER also promotes the occurrence and development of uterine adenomyosis through other pathways.

Potential mechanisms of an antiadenomyosis chinese herbal formula shaoyao-gancao decoction in primary cell culture model.

Background. Shaoyao-Gancao Decoction (SGD), a well-known traditional Chinese medicine prescription, has been widely used to treat adenomyosis, dysmenorrhea, abdominal pain, and inflammation in Asia. However, the mechanism underlying the effectiveness of SGD in the treatment of adenomyosis still remains elusive. The present study aimed to investigate the bioactivity of SGD and its underlying molecular mechanisms using cultured human adenomyosis-derived cells. Methods. Human adenomyosis-derived cells were treated with SGD and its major constituents (paeoniflorin and liquiritin) in vitro. Effects of SGD, paeoniflorin, and liquiritin on cell proliferation and apoptosis were examined by MTT assay and flow cytometry analyses. The effects of SGD, paeoniflorin, and liquiritin on the production of PGE2 and PGF2α were assayed using ELISA. ER-α and OTR mRNA expression levels were also evaluated by real-time qRT-PCR. Results. SGD, paeoniflorin, and liquiritin inhibited proliferation and induced apoptosis of human adenomyosis-derived cells in a dose-dependent manner. SGD and paeoniflorin significantly reduced the PGE2 and PGF2α production. Furthermore, they remarkably decreased the mRNA levels of ER-α and OTR. Conclusions. The results of this study provide possible mechanisms for the bioactivity of SGD for treating adenomyosis and contribute to the ethnopharmacological knowledge about this prescription.