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Research Paper|Volume 11, Issue 19|pp 8362—8373

Mogroside V protects porcine oocytes from in vitro ageing by reducing oxidative stress through SIRT1 upregulation

Junyu Nie1,2, Lumin Sui1,2, Huiting Zhang1,2, Hengye Zhang1,2, Ke Yan1,2, Xiaogan Yang1,2, Shengsheng Lu1,2, Kehuan Lu1,2, Xingwei Liang1,2
  • 1State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources, Guangxi University, Nanning 530004, Guangxi, China
  • 2College of Animal Science and Technology, Guangxi University, Nanning 530004, Guangxi, China
Received: August 14, 2019Accepted: September 22, 2019Published: October 6, 2019
https://doi.org/10.18632/aging.102324

Copyright © 2019 Nie et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Postovulatory ageing compromises oocyte quality and subsequent development in various manners. We aimed to assay the protective effects of mogroside V on porcine oocyte quality during in vitro ageing and explore the related causes. We observed that mogroside V can effectively maintain normal oocyte morphology and early embryo development competence after prolonged culture for 24 h. Moreover, mogroside V can markedly reduce reactive oxygen species (ROS) levels, alleviate spindle formation and chromosome alignment abnormalities, improve mitochondrial contents, adenosine triphosphate (ATP) levels and the membrane potential (ΔΨm), and reduce early apoptosis in aged oocytes. We examined the molecular changes and found that SIRT1 expression was decreased in in vitro aged oocytes but was maintained by exposure to mogroside V. However, when SIRT1 was successfully inhibited by the specific inhibitor EX-527, mogroside V could not reduce ROS levels or alleviate abnormal spindle organization and chromosome misalignment. In summary, our results demonstrated that mogroside V can alleviate the deterioration of oocyte quality during in vitro ageing, possibly by reducing oxidative stress through SIRT1 upregulation.