Department of Obstetrics and Gynecology, University of California, Davis, 4860 Y Street, Sacramento, California 95817, USA.
Endocrinology. 2012 Aug;153(8):4019-29. doi: 10.1210/en.2012-1385. Epub 2012 Jun 19.
Polycystic ovary syndrome is characterized by theca-interstitial hyperplasia and increased expression of steroidogenic genes, leading to excessive androgen production. Resveratrol, a natural polyphenol, promotes apoptosis and reduces rat theca-interstitial cell growth, in part by inhibiting the mevalonate pathway and decreasing the availability of substrates of isoprenylation [farnesyl-pyrophosphate (FPP) and geranylgeranyl-pyrophosphate (GGPP)]. This study evaluated the effect of resveratrol on rat theca-interstitial cell steroidogenesis. Because resveratrol may activate sirtuins, this study also investigated whether steroidogenesis was affected by sirtuin inhibitors (nicotinamide, sirtinol). Theca-interstitial cells were cultured with or without resveratrol (1-10 μm), GGPP (30 μm), FPP (30 μm), nicotinamide (1 mm), and/or sirtinol (10 μm). Resveratrol did not affect progesterone levels but reduced androgen production in a concentration-dependent fashion (androstenedione by up to 78% and androsterone by up to 76%). This inhibitory effect correlated with a decrease in mRNA expression of genes regulating androgen production, especially Cyp17a1 (by up to 73%). GGPP and FPP had no effect on androgen levels and Cyp17a1 mRNA levels and did not alter the effects induced by resveratrol. Similarly, sirtuin inhibitors did not reverse resveratrol-induced inhibition of steroidogenesis. However, resveratrol decreased activity of serine-threonine kinase/protein kinase B pathway, a cell-signaling pathway involved in ovarian steroidogenesis. The present findings indicate that resveratrol reduces androgen production primarily by inhibiting Cyp17a1 mRNA expression, and this inhibition may be mediated, in part, by blocking the activity of the serine-threonine kinase/protein kinase B pathway. These findings may be of clinical relevance to conditions associated with excessive production of androgens by theca cells, such as polycystic ovary syndrome.
多囊卵巢综合征的特征是间质增生和类固醇生成基因表达增加,导致雄激素产生过多。白藜芦醇是一种天然多酚,可促进细胞凋亡并减少大鼠间质细胞生长,部分通过抑制甲羟戊酸途径和减少异戊烯基化底物(法呢基焦磷酸(FPP)和香叶基焦磷酸(GGPP))的可用性。本研究评估了白藜芦醇对大鼠间质细胞类固醇生成的影响。由于白藜芦醇可能激活沉默调节蛋白,因此本研究还研究了类固醇生成是否受沉默调节蛋白抑制剂(烟酰胺、sirtinol)的影响。用或不用白藜芦醇(1-10μm)、GGPP(30μm)、FPP(30μm)、烟酰胺(1mm)和/或 sirtinol(10μm)培养间质细胞。白藜芦醇不影响孕酮水平,但以浓度依赖的方式降低雄激素的产生(雄烯二酮高达 78%,雄酮高达 76%)。这种抑制作用与调节雄激素产生的基因的 mRNA 表达减少相关,特别是 Cyp17a1(高达 73%)。GGPP 和 FPP 对雄激素水平和 Cyp17a1 mRNA 水平没有影响,也没有改变白藜芦醇诱导的作用。同样,沉默调节蛋白抑制剂也不能逆转白藜芦醇诱导的类固醇生成抑制。然而,白藜芦醇降低了丝氨酸-苏氨酸激酶/蛋白激酶 B 通路的活性,该通路是参与卵巢类固醇生成的细胞信号通路。本研究结果表明,白藜芦醇主要通过抑制 Cyp17a1 mRNA 表达来减少雄激素的产生,这种抑制可能部分通过阻断丝氨酸-苏氨酸激酶/蛋白激酶 B 通路的活性来介导。这些发现可能与过多的间质细胞产生雄激素的疾病有关,如多囊卵巢综合征。