Rostami Dovom Marzieh, Noroozzadeh Mahsa, Mosaffa Nariman, Piryaei Abbas, Zadevakili Azita, Amin Abdollahifar Mohammad, Ramezani Tehrani Fahimeh
Reproductive Endocrinology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Int J Reprod Biomed. 2022 May 23;20(4):319-330. doi: 10.18502/ijrm.v20i4.10904. eCollection 2022 Apr.
Premature ovarian insufficiency (POI) affects about 1% of women of reproductive ages (15-45 yr), with no curative treatment.
We aimed to present a rat model of POI using a D-galactose enriched diet.
In a pilot study, 4 pregnant Wistar rats were divided into 4 groups; 3 groups were fed galactose-enriched diets at days 3-15 of pregnancy (G1); on the 3 day of pregnancy to parturition (G2), and the 3 day of pregnancy until the end of the weaning period (G3). Also, group 4, as the control group (G0), was fed standard pellets during the study. After confirming the lack of adverse effects of dieting with galactose in terms of offsprings' birth weight, we performed our study designed the same as the pilot study. A total of 40 pregnant Wistar rats were randomly divided into 4 groups. Ovarian histology, reproductive hormones, and immunological characteristics of the female offspring were examined in all experimental groups and compared.
The pilot study revealed no significant differences in the birth weight of the offspring of the 4 study groups (p = 0.96). The ovarian index in the female offspring of those with a gal-exposed diet was significantly lower than that of the control group offspring (p 0.01).
As the birth weights of the offspring of our experimental and control groups were similar, it can be concluded that the reduction of ovarian follicles after prenatal exposure to D-galactose is due to the ovotoxicity of galactose. The results of our final study will provide more information about the rat POI model induced by prenatal exposure to D-galactose.
卵巢早衰(POI)影响约1%的育龄女性(15 - 45岁),且尚无治愈方法。
我们旨在建立一种使用富含D - 半乳糖饮食的大鼠卵巢早衰模型。
在一项初步研究中,将4只怀孕的Wistar大鼠分为4组;3组在妊娠第3 - 15天(G1)、妊娠第3天至分娩(G2)、妊娠第3天至断奶期末(G3)喂食富含半乳糖的饮食。此外,第4组作为对照组(G0),在研究期间喂食标准颗粒饲料。在确认半乳糖饮食对后代出生体重无不良影响后,我们按照与初步研究相同的设计进行了本研究。总共40只怀孕的Wistar大鼠被随机分为4组。对所有实验组的雌性后代进行卵巢组织学、生殖激素和免疫特性检查并进行比较。
初步研究显示4个研究组后代的出生体重无显著差异(p = 0.96)。暴露于半乳糖饮食的雌性后代的卵巢指数显著低于对照组后代(p < 0.01)。
由于我们实验组和对照组后代的出生体重相似,可以得出结论,产前暴露于D - 半乳糖后卵巢卵泡减少是由于半乳糖的卵巢毒性。我们最终研究的结果将提供更多关于产前暴露于D - 半乳糖诱导的大鼠卵巢早衰模型的信息。