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口服牡蛎多肽可保护 C57BL/6 小鼠的卵巢免受 D-半乳糖诱导的卵巢早衰。

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

机构信息

Department of Engineering and Applied Biology, College of Life Science, Sichuan Agricultural University, Ya'an, China.

Ningbo Bofeng Biological Science and Technology Co., Ltd, Zhejiang, China.

出版信息

J Sci Food Agric. 2020 Jan 15;100(1):92-101. doi: 10.1002/jsfa.9997. Epub 2019 Sep 30.

Abstract

BACKGROUND

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.

RESULTS

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).

CONCLUSION

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.

摘要

背景

牡蛎多肽具有多种生物功能,如抗癌和抗氧化应激,但它是否对原发性卵巢功能衰竭(POF)有保护作用尚不清楚。为了解决这个问题,我们基于半乳糖诱导的 C57BL/6 雌性小鼠 POF 模型,用牡蛎多肽进行每日灌胃,研究其保护作用。

结果

牡蛎多肽恢复了不规则发情周期和血清卵泡刺激素(FSH)、黄体生成素(LH)和孕酮(P)水平的异常,以及半乳糖诱导的 Amh mRNA 表达水平的降低。口服牡蛎多肽可改善 POF 小鼠的卵泡发育,增加原始卵泡比例,减少闭锁卵泡数量。此外,在牡蛎多肽处理的小鼠中,总超氧化物歧化酶(T-SOD)活性显著增加,而丙二醛水平显著降低。应激相关基因(SOD2、SIRT1 和 FOXO3a)的 mRNA 表达水平在半乳糖诱导后显著上调,但经牡蛎多肽灌胃后,上调减弱或消失。此外,牡蛎多肽处理还减少了卵巢颗粒细胞的凋亡,并下调了凋亡相关基因(p53 和 Bad,但不是 Bcl-2)的 mRNA 表达水平。

结论

本研究表明,牡蛎多肽可能通过其抗氧化应激活性保护卵巢免受半乳糖诱导的 POF,从而挽救半乳糖诱导的卵巢氧化损伤,防止卵巢细胞凋亡,从而使 POF 引发的异常接近正常水平。© 2019 化学工业协会。

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