| Objective: To investigate the expression of the aromatase p450arom, estradiol, estrogen receptor mRNA (ERmRNA) and the suppressive effect of aromatase inhibitor exemestane on the proliferation of the stromal cells of ectopic endometrium in vitro. Methods: The eutopic and ectopic endometrial stromal cell were cultured in vitro and be divided into four subgroups, exemestane group, exemestane plus estradiol group, 0.5% ethanol group and control group, respectively. The concentration of estradiol in media supernatant was measured by immunofluorometry. MTT was used to examine the proliferative activity of ectopic stromal cell, and RT-PCR was used to determine the expression of the aromatase and estrogen receptor mRNA. Results: There was no the expression of the aromatase in normal endometrium. The expression levels of the aromatase, estradiol and estrogen receptor mRNA in the ectopic endometrium was higher than that of the eutopic endometrium (P<0.05). Low dosage (6 × 10-9mol/L) of exemestane had no effect on the expression of p450arom and ERmRNA, and estradiol synthesis in the ectopic stromal cell. However, high dosage (6 × 10-8mol/L - 6× 10-7mol/L) of exemestane could down-regulate the expression of p450arom, and to inhibit estradiol synthesis and the proliferation activity of the ectopic stromal cell, but the expression of ERmRNA had no change. Estrogencould block the suppressive effect of aromatase inhibitor exemestane on the ectopic stromal cell. The proliferative activity of ethanol group and control group had no significant difference(P>0.05). Conlusions: There was no the expression of the aromatase in normal endometrium. The proliferation activity of the ectopic stromal cell was associated with the higher expression of aromatase p450arom, ERmRNA and increased production of estradiol in vitro. Aromatse inhibitor exemestane could suppress the proliferation of ectopic stromal cell in the time-dosage-dependent manner by down-regulating the expression of the aromatase p450arom and reducing the estradiol synthesis. Estrogen could block the effect of aromatase on the ectopic stromal cell.Objective: To investigate the changes of the genes and cytokines which was associated with the apoptosis pathway of stromal cell of ectopic endometrium, and the effect of the aromatase and it's inhibitor exemestane. Methods: The normal and ectopic endometrial stromal cells were cultured in vitro, and be divided into three groups:exemestane group; (Dexemestane plus estradiol group; ?control group. When the ectopic endometrial stromal cells were cultured with aromatase inhibitor exemestane for 72h, the rate of cellular apoptosis and the phase of cellular cycle were measured by FCM. Immunohistochemistry and RT-PCR were used to determine the expression of the genes and cytokines including bax, bcl-2, caspase-3, -8, -9, survivin and P-endorphin which was associated with the signal pathway of cellular apoptosis. Results: Comparison with normal endometrium, the expression of bcl-2, survivin and estradiol was enhanced, but the the expression of bax, caspase-3, -8, -9, P-endorphin and the apoptosis activity was decreased in the stromal cell of ectopic endometrium (P<0.05). Aromatase inhibitor exemestane enhanced the expression of Bax, caspase-3, -9 and P -endorphin (PO.05), and down-regulating the expression of bcl-2 and survivin, and enhancing the apoptosis activity of ectopic stromal cells (P<0.05), but the expression of caspase 8 was not affected. The expression of bcl-2, surviving, Bax, caspase-3, -8, -9 and 3 -endorphin of ectopic stromal cells which was cultured with co-culturing of exemestane and estradiol was not significant change. Conclusions: The reduced apoptosis activity of ectopic stromal cells was associatedwith the expression enhancement of bcl-2 and survivin and expression decrease of bax, caspase-3, -8, -9 and P -endorphin. Aromatase inhibitor exemestane enhanced the apoptosis activity of ectopic stromal cells by up-regulating the expression of bax, caspase-3? -8, -9 and ￡ -endorphin, and down-regulating the expression of bcl-2, survivin and estrogen synthesis. Estrogen could block the effect of aromatase inhibitor exemestane on the ectopic stromal cells. Objective: To investigate the relationship between the expression of metalloproteinase-2 ,-14, TIMP-2, CD44s and the invasive growth of stromal cells of ectopic endometrium, and to explore the suppressive effect of aromatase inhibitor exmestane on the proliferation and invasive growth of ectopic stromal cell in vitro. Methods: the stromal cells of normal endometrium and ectopic endometrium were cultured with aromatase inhibitor exemestane (6xlO"8mol/L) and estradiol (2.5><10"10mol/L) in vitro, and the changes of the expression of matrix metalloproteinase-2, -14, tissue inhibitor metalloproteinase-2 (TIMP-2) and CD44smRNA in stromal cells was observed. RT-PCR was used to measure the expression of CD44s, and the immunohistochemistry was used to examine the expression of MMP-2, -14 and TIMP-2. Results: Comparison with normal endometrium, the expression of CD44smRNA, MMP-2, -14 was enhanced, and the expression of TIMP-2 was decreased in the stromal cell of ectopic endometrium. Aromatase inhibitor exemestane could decrease the expression of CD44smRNA, MMP-2, -14, but could enhance the expression of TIMP-2. The expression of CD44smRNA , MMP-2 ^ -14 was positive correlation to the levels of estradiol, but the expression of TIMP-2 was negative correlation to the levels of estradiol; The expression between MMP-2 and MMP14 was positive correlation, but negative correlation with the expression of TIMP-2. Conclusions: The invasive growth of the stromal cell of ectopic endometrium was associated with the high expression of MMP-2, MMP-14, CD44smRNA, and the low expression of TIMP-2. Aromatase inhibitor exemestane could suppress the proliferation and...
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