Enhancing antioxidant capacity via NRF2 pathway activation to mitigate heat stress-induced oxidative damage in bovine granulosa cells, oocytes, and embryos

通过激活NRF2通路增强抗氧化能力,以减轻热应激引起的牛颗粒细胞、卵母细胞和胚胎的氧化损伤

阅读:2

Abstract

Global warming-induced thermal stress is an escalating threat to livestock fertility, perturbing ovarian function, oocyte maturation, and preimplantation embryo development through excessive accumulation of reactive oxygen species (ROS), which drive follicular oxidative damage. Although embryo transfer technologies offer a practical abatement strategy for mitigating such implications caused by HS, in vitro systems lack the endogenous antioxidant defenses present in vivo, leaving follicular cells, gametes, and embryos particularly vulnerable. Here, we aimed to investigate whether antioxidants, including quercetin (QUE), carnosol (CAR), and sulforaphane (SFN), mitigate HS-induced follicular oxidative damage in bovine granulosa cells (GCs), oocytes, and embryos. For this, antioxidant supplementation, either individually or in combination, was performed during in vitro GC culture and oocyte maturation under normothermic (NT) or HS conditions. Across all models, QUE and SFN supplementation activated nuclear NRF2, reduced ROS accumulation, and restored mitochondrial function and apoptosis levels under conditions of HS. In oocytes exposed to thermal stress, QUE and SFN supplementation also led to increased blastocyst rates and total cell numbers. Single-embryo metabolic profiling revealed reduced oxygen consumption (OCR) and extracellular acidification (ECAR) rates in blastocysts derived from antioxidant-treated oocytes, indicative of enhanced metabolic efficiency. Moreover, quantitative analysis of recently defined embryo competence-associated genes demonstrated a restoration of the embryo competence index (ECI) following QUE and SFN supplementation. In conclusion, antioxidant supplementation during GC culture and oocyte maturation alleviates HS-induced reproductive dysfunction by restoring redox homeostasis, preserving metabolic efficiency, and re-establishing embryo competence, thereby providing a mechanistically grounded strategy to mitigate climate-driven fertility decline in cattle.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。