Apigenin delays postovulatory oocyte aging by reducing oxidative stress through SIRT1 upregulation.

Theriogenology

Guangdong Provincial Key Laboratory of Large Animal Models for Biomedicine, School of Biotechnology and Health Sciences, Wuyi University, Jiangmen, China; Research and Development Department, Qingdao Haier Biotech Co. Ltd, Qingdao, China. Electronic address:

Published: April 2024

AI Article Synopsis

  • After ovulation, aging porcine oocytes suffer from decreased quality and development defects, but the flavonoid apigenin (API) shows potential protective effects.
  • API treatment lowers activation rates and mitigates oxidative damage by reducing reactive oxygen species and improving mitochondrial function, along with boosting glutathione and ATP levels.
  • The study found that API enhances embryonic development rates in aged oocytes and helps preserve oocyte quality by upregulating sirtuin 1, which declines with aging.

Article Abstract

After ovulation, senescent oocytes inevitably experience reduced quality and defects in embryonic development. Apigenin (API) is a flavonoid with a wide range of pharmacological effects. Therefore, this study examined the protective effects of API on the quality of porcine oocytes during in-vitro ageing and the underlying mechanisms. The results showed that API treatment could reduce the activation rate after aging for 48 h. In addition, API significantly reduced reactive oxygen species, abnormal distribution of mitochondria, early apoptosis in ageing oocytes, increased glutathione, and mitochondrial adenosine triphosphate levels in ageing oocytes. Importantly, API increased the embryonic development rate in aged oocytes. We also examined molecular changes, finding decreased sirtuin 1 expression in in-vitro postovulatory oocytes, but API reversed this effect. Our results suggest that API attenuates the deterioration of oocyte quality during in-vitro ageing, possibly by reducing oxidative stress through the upregulation of sirtuin 1.

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Source
http://dx.doi.org/10.1016/j.theriogenology.2024.01.007DOI Listing

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