Pubertal ovarian function might be dependent on the factors present in the pre-pubertal stages. Visfatin regulates ovarian steroidogenesis in adult. To date, no study has investigated the role of visfatin either in pre-pubertal or pubertal mice ovary. Thus, we investigated the role of visfatin in pre-pubertal mice ovary in relation to steroidogenesis and proliferation and apoptosis in vitro by inhibiting the endogenous visfatin by a specific inhibitor, FK866. Inhibition of visfatin increased the estrogen secretion and also up-regulated the expression of CYP11A1, 17βHSD and CYP19A1 in mice ovary. Furthermore, active caspase3 was up-regulated along with the down-regulation of BAX and BCL2 in the pre-pubertal ovary after visfatin inhibition. The expression of GCNA, PCNA, and BrdU labeling was also decreased by FK866 treatment. These results suggest that visfatin inhibits steroidogenesis, increases proliferation, and suppresses apoptosis in the pre-pubertal mice ovary. So, visfatin is a new regulator of ovary function in pre-pubertal mice.

青春期卵巢功能可能取决于青春期前阶段存在的因素。Visfatin调节成人卵巢类固醇生成。迄今为止，尚无研究调查visfatin在青春期前或青春期小鼠卵巢中的作用。因此，我们研究了关系内脂素在青春期前小鼠卵巢的作用，类固醇激素合成和细胞增殖和凋亡体外通过特异性抑制剂FK866抑制内源性visfatin。抑制visfatin可以增加雌性激素的分泌，并上调CYP11A1、17βHSD和CYP19A1在小鼠卵巢中的表达。此外，visfatin抑制后，青春期前卵巢中的活性caspase3随BAX和BCL2的下调而上调。FK866处理还降低了GCNA，PCNA和BrdU标记的表达。这些结果表明，visfatin在青春期前小鼠卵巢中抑制类固醇生成，增加增殖并抑制细胞凋亡。因此，visfatin是青春期前小鼠卵巢功能的新调节剂。