Forneris M, Rosales E, Ciuffo G, Oliveros L
Laboratorio de Biología de la Reproducción, Facultad de Química, Bioquímica y Farmacia, Universidad Nacional de San Luis, San Luis, Argentina.
Horm Metab Res. 2008 Apr;40(4):239-44. doi: 10.1055/s-2007-1022545. Epub 2008 Feb 6.
The functional relationship between the ovary and immune cells is well known. The modulation of ovarian steroidogenesis in adult rats with polycystic ovary (PCO) by secretions of cultured splenocytes treated with 10 (-6) M testosterone or 10 (-6) M testosterone plus 10 (-4) M flutamide, an androgen receptor antagonist, was investigated. Polycystic ovary was induced by estradiol valerate (2 mg/rat). Polycystic ovary splenocyte secretions decreased the release of androstenedione from PCO ovaries in contrast to the effect of non-PCO splenocyte secretions. This decrease was associated with a significant decrease in androgen receptor and IL-12 mRNA expression in PCO splenocytes. When splenocytes were treated with testosterone, their conditioned media further decreased androstenedione release from the ovary and had a greater inhibitory effect on PCO ovary compared with non-PCO ovary. This effect was reversed by flutamide. Polycystic ovary splenocytes showed a decrease in IL-1 beta mRNA expression. Their secretions scarcely affected progesterone release from non-PCO ovaries but significantly stimulated progesterone release from PCO ovary by an androgen-independent mechanism. The differential steroidogenic ability of splenocyte secretions from PCO rats is associated with the IN VITRO testosterone environment. Polycystic ovary splenocytes might exert a protective action against PCO effects through their secretions by inducing a low androstenedione response from the ovary.
卵巢与免疫细胞之间的功能关系已为人熟知。本研究探讨了用10（-6）M睾酮或10（-6）M睾酮加10（-4）M氟他胺（一种雄激素受体拮抗剂）处理的培养脾细胞分泌物对成年多囊卵巢（PCO）大鼠卵巢类固醇生成的调节作用。戊酸雌二醇（2mg/大鼠）诱导多囊卵巢。与非PCO脾细胞分泌物的作用相反，多囊卵巢脾细胞分泌物减少了PCO卵巢中雄烯二酮的释放。这种减少与PCO脾细胞中雄激素受体和IL-12 mRNA表达的显著降低有关。当脾细胞用睾酮处理时，其条件培养基进一步降低了卵巢中雄烯二酮的释放，并且与非PCO卵巢相比，对PCO卵巢具有更大的抑制作用。氟他胺可逆转这种作用。多囊卵巢脾细胞显示IL-1βmRNA表达降低。它们的分泌物几乎不影响非PCO卵巢中孕酮的释放，但通过一种不依赖雄激素的机制显著刺激PCO卵巢中孕酮的释放。PCO大鼠脾细胞分泌物的不同类固醇生成能力与体外睾酮环境有关。多囊卵巢脾细胞可能通过其分泌物诱导卵巢产生低雄烯二酮反应，从而对PCO效应发挥保护作用。
