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Oral oyster polypeptides protect ovary against d‐galactose‐induced premature ovarian failure in C57BL/6 mice

牡蛎 卵巢早衰 内科学 氧化应激 内分泌学 毛囊 细胞凋亡 促黄体激素 促卵泡激素 生物 丙二醛 超氧化物歧化酶 卵泡 男科 卵巢 卵泡发生 激素 生物化学 医学 基因 渔业 胚胎发生
作者
Yunkun Li,Wei Qiu,Zhi Zhang,Xingfa Han,Guixian Bu,Fengyan Meng,Fanli Kong,Xiaohan Cao,Anqi Huang,Zhijiang Feng,Yun Li,Xianyin Zeng,Xiaogang Du
出处
期刊:Journal of the Science of Food and Agriculture [Wiley]
卷期号:100 (1): 92-101 被引量:25
标识
DOI:10.1002/jsfa.9997
摘要

Oyster polypeptides have various biofunctions, such as anti-cancer and anti-oxidative stress, but whether it has the protective effects to primary ovarian failure (POF) remains poorly understand. To address this issue, daily gavage of oyster polypeptides was performed to investigate their protective effect, basing on d-galactose-induced POF model in C57BL/6 female mice.Oyster polypeptides restored the irregular estrous cycles and the abnormal serum follicle stimulating hormone (FSH), luteinizing hormone (LH) and progesterone (P) levels as well as the decreased mRNA expression level of Amh that were induced by d-galactose. The follicle development of POF mice was improved by increasing the primordial follicle ratio and decreasing the atretic follicle number after oral administration of oyster polypeptides. Moreover, in the oyster polypeptides treated mice, the total superoxide dismutase (T-SOD) activity was significantly increased, while the malondialdehyde levels were significantly decreased. The mRNA expression levels of stress-related genes (SOD2, SIRT1 and FOXO3a) were remarkably up-regulated after d-galactose induction, but the up-regulation was weakened or disappeared by the gavage of oyster polypeptides. In addition, oyster polypeptides treatment also reduced the apoptosis of the ovarian granulosa cells and down-regulated the mRNA expression levels of apoptosis-related genes (p53 and Bad but not Bcl-2).This study reveals that oyster polypeptides may protect ovary against d-galactose-induced POF by their anti-oxidative stress activity to rescue d-galactose-induced ovarian oxidative damage and therefore to prevent ovarian cells apoptosis, thereby tipping the abnormality trigged by POF to get close to the normal levels. © 2019 Society of Chemical Industry.
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