Isono Wataru, Wada-Hiraike Osamu, Kawamura Yumiko, Fujii Tomoyuki, Osuga Yutaka, Kurihara Hiroki
1 Department of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
2 Department of Physiological Chemistry and Metabolism, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Reprod Sci. 2018 Sep;25(9):1413-1423. doi: 10.1177/1933719117746758. Epub 2017 Dec 13.
Age-related fertility decline is hypothesized to occur mainly by the spontaneous exhaustion and deterioration of the ovarian follicle, and the accumulation of ovarian tissue damage resulting from the ovulation cycle may play roles in the process. In this study, we hypothesized that suppressing ovulation would exert protective effects against age-related fertility decline. To test this hypothesis, we established a mouse model in which oral contraceptives (OCs) were administered daily. Female C57BL/6N mice were administered OCs daily from the age of 2 months to 12 months as an ovulation suppression mouse model. Mouse fecundity was investigated by counting oocyte number after ovarian stimulation and by examining live fetuses after mating. We found that compared with control mice administered vehicle alone, 12-month-old mice administered 2-fold dose OCs used for treating humans exhibited a significantly greater average oocyte number after ovarian stimulation (8.5 ± 0.6 vs 5.9 ± 0.6, P < .01). In addition, spontaneous conception with living fetuses after mating was strikingly increased in 12-month-old mice administered OCs relative to controls (6.0 ± 1.2 vs 0.4 ± 0.3, P < .01). In the histological examination of mouse ovarian tissues, we did not detect a significant difference in ovarian follicle number, but reduced amount of brownish foamy fibrous tissues, which might reflect ovarian tissue damage, was detected in aged mice administered OCs. These results suggest the possibility that long-term OC administration might alleviate age-related fertility decline, and the improvement mechanism could be attributed to the prevention of ovarian tissue damage by suppressing ovulation.
年龄相关性生育力下降被认为主要是由于卵巢卵泡的自然耗竭和退化,并且排卵周期导致的卵巢组织损伤积累可能在这一过程中起作用。在本研究中,我们假设抑制排卵对年龄相关性生育力下降具有保护作用。为了验证这一假设,我们建立了一个每天给予口服避孕药(OCs)的小鼠模型。将雌性C57BL/6N小鼠从2月龄至12月龄每天给予OCs作为排卵抑制小鼠模型。通过在卵巢刺激后计数卵母细胞数量以及在交配后检查活胎来研究小鼠的生育力。我们发现,与仅给予赋形剂的对照小鼠相比,给予用于治疗人类剂量2倍的OCs的12月龄小鼠在卵巢刺激后平均卵母细胞数量显著更多(8.5±0.6对5.9±0.6,P<.01)。此外,给予OCs的12月龄小鼠与对照相比,交配后活胎的自然受孕显著增加(6.0±1.2对0.4±0.3,P<.01)。在小鼠卵巢组织的组织学检查中,我们未检测到卵巢卵泡数量有显著差异,但在给予OCs的老年小鼠中检测到褐色泡沫状纤维组织的量减少,这可能反映了卵巢组织损伤。这些结果提示长期给予OCs可能减轻年龄相关性生育力下降的可能性,并且改善机制可能归因于通过抑制排卵预防卵巢组织损伤。