Luchetti Carolina Griselda, Solano Maria Emilia, Sander Valeria, Arcos Maria L Barreiro, Gonzalez Claudio, Di Girolamo Guillermo, Chiocchio Sara, Cremaschi Graciela, Motta Alicia B
Laboratorio de Fisiopatología Ovárica, Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Serrano 669, C1414DEM Buenos Aires, Argentina.
J Reprod Immunol. 2004 Dec;64(1-2):59-74. doi: 10.1016/j.jri.2004.04.002.
The purpose of the present report was to study the possible relationship between ovarian functionality and the immune response during cystogenesis induced by androgenization with dehydroepiandrosterone (DHEA). Daily injection of DHEA (6 mg/kg body weight) for 20 consecutive days induced ovarian cysts in BALB/c mice. As markers of ovarian function, serum estradiol (E) and progesterone (P) and the ovarian inmunomodulator prostaglandin E (PGE) were analyzed. In order to know how the integrity of the tissue was altered after induction of cystogenesis, the oxidative status was also evaluated. Serum E and P levels, and ovarian PGE concentration, were increased in animals with cysts compared with healthy controls. The oxidant status (quantified by malondialdehyde (MDA) formed after the breakdown of the cellular membrane by free radical mechanisms) was augmented, meanwhile the antioxidant (evaluated by the glutathione (GSH) content) diminished during the induction of cystogenesis. Both immunohistochemical and flow cytometry assays demonstrated that DHEA treatment increased the number of T lymphocytes infiltrating ovarian tissue. Therefore, while ovarian controls showed equivalent expression of CD4+ and CD8+ T cell subsets, injection of DHEA yielded a selective ovarian T cell infiltration as demonstrated by enhanced CD8+ and diminished CD4+ T lymphocyte expression. These results show that the development of cysts involves changes in ovarian function and an imbalance in the oxidant-antioxidant equilibrium. We observed also both an increased and selective T lymphocyte infiltration.
本报告的目的是研究在脱氢表雄酮（DHEA）雄激素化诱导囊肿形成过程中，卵巢功能与免疫反应之间的可能关系。连续20天每天给BALB/c小鼠注射DHEA（6毫克/千克体重）可诱导卵巢囊肿形成。分析血清雌二醇（E）、孕酮（P）以及卵巢免疫调节因子前列腺素E（PGE）作为卵巢功能的标志物。为了了解囊肿形成诱导后组织完整性如何改变，还评估了氧化状态。与健康对照组相比，有囊肿的动物血清E和P水平以及卵巢PGE浓度升高。在囊肿形成诱导过程中，氧化状态（通过自由基机制导致细胞膜分解后形成的丙二醛（MDA）定量）增强，同时抗氧化剂（通过谷胱甘肽（GSH）含量评估）减少。免疫组织化学和流式细胞术检测均表明，DHEA处理增加了浸润卵巢组织的T淋巴细胞数量。因此，虽然卵巢对照组显示CD4 +和CD8 + T细胞亚群表达相当，但注射DHEA导致卵巢T细胞选择性浸润，表现为CD8 + T淋巴细胞表达增强而CD4 +减少。这些结果表明，囊肿的形成涉及卵巢功能变化以及氧化-抗氧化平衡失衡。我们还观察到T淋巴细胞浸润增加且具有选择性。
