Quercetin protects porcine oocytes from in vitro aging by reducing oxidative stress and maintaining the mitochondrial functions

Jiao, Yafei; Wang, Yixian; Jiang, Tao; Wen, Keying; Cong, Peiqing; Chen, Yaosheng; He, Zuyong

doi:10.3389/fcell.2022.915898

Cited by 4 publications

(1 citation statement)

References 37 publications

(40 reference statements)

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“…Research has shown that multiple antioxidants can restore mitochondrial function by reducing ROS production and stimulating antioxidant production. It mainly includes coenzyme Q10 ( 177 ), vitamin E ( 164 ), vitamin C ( 164 ), L-carnitine ( 165 , 166 ), melatonin ( 167 , 168 ), quercetin ( 169 ), resveratrol ( 170 ), astaxanthin ( 171 ), and ginsenoside Rb1 ( 44 ).…”

Section: Methods To Slow Down Ovarian Aging and Prolong Reproductive ...mentioning

confidence: 99%

Mechanisms of mitochondrial dysfunction in ovarian aging and potential interventions

Ju,

Zhao,

et al. 2024

Front. Endocrinol.

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Mitochondria plays an essential role in regulating cellular metabolic homeostasis, proliferation/differentiation, and cell death. Mitochondrial dysfunction is implicated in many age-related pathologies. Evidence supports that the dysfunction of mitochondria and the decline of mitochondrial DNA copy number negatively affect ovarian aging. However, the mechanism of ovarian aging is still unclear. Treatment methods, including antioxidant applications, mitochondrial transplantation, emerging biomaterials, and advanced technologies, are being used to improve mitochondrial function and restore oocyte quality. This article reviews key evidence and research updates on mitochondrial damage in the pathogenesis of ovarian aging, emphasizing that mitochondrial damage may accelerate and lead to cellular senescence and ovarian aging, as well as exploring potential methods for using mitochondrial mechanisms to slow down aging and improve oocyte quality.

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Section: Methods To Slow Down Ovarian Aging and Prolong Reproductive ...mentioning

confidence: 99%

Mechanisms of mitochondrial dysfunction in ovarian aging and potential interventions

Ju,

Zhao,

et al. 2024

Front. Endocrinol.

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Cordycepin delays postovulatory aging of oocytes through inhibition of maternal mRNAs degradation via DCP1A polyadenylation suppression

Li,

Zhu,

Liu

et al. 2023

Cell. Mol. Life Sci.

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Postovulatory aging leads to the decline in oocyte quality and subsequent impairment of embryonic development, thereby reducing the success rate of assisted reproductive technology (ART). Potential preventative strategies preventing oocytes from aging and the associated underlying mechanisms warrant investigation. In this study, we identified that cordycepin, a natural nucleoside analogue, promoted the quality of oocytes aging in vitro, as indicated by reduced oocyte fragmentation, improved spindle/chromosomes morphology and mitochondrial function, as well as increased embryonic developmental competence. Proteomic and RNA sequencing analyses revealed that cordycepin inhibited the degradation of several crucial maternal proteins and mRNAs caused by aging. Strikingly, cordycepin was found to suppress the elevation of DCP1A protein by inhibiting polyadenylation during postovulatory aging, consequently impeding the decapping of maternal mRNAs. In humans, the increased degradation of DCP1A and total mRNA during postovulatory aging was also inhibited by cordycepin. Collectively, our findings demonstrate that cordycepin prevents postovulatory aging of mammalian oocytes by inhibition of maternal mRNAs degradation via suppressing polyadenylation of DCP1A mRNA, thereby promoting oocyte developmental competence.

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Protective effect of onion peel extract on ageing mouse oocytes

Guo-bo

et al. 2023

Zygote

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Summary Mammalian oocytes not fertilized immediately after ovulation can undergo ageing and a rapid decline in quality. The addition of antioxidants can be an efficient approach to delaying the oocyte ageing process. Onion peel extract (OPE) contains quercetin and other flavonoids with natural antioxidant activities. In this study, we investigated the effect of OPE on mouse oocyte ageing and its mechanism of action. The oocytes were aged in vitro in M16 medium for 16 h after adding OPE at different concentrations (0, 50, 100, 200, and 500 μg/ml). The addition of 100 μg/ml OPE reduced the oocyte fragmentation rate, decreased the reactive oxygen species (ROS) level, increased the glutathione (GSH) level, and improved the mitochondrial membrane potential compared with the control group. The addition of OPE also increased the expression of SOD1, CAT, and GPX3 genes, and the caspase-3 activity in OPE-treated aged oocytes was significantly lower than that in untreated aged oocytes and similar to that in fresh oocytes. These results indicated that OPE delayed mouse oocyte ageing by reducing oxidative stress and apoptosis and enhancing mitochondrial function.

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Quercetin protects porcine oocytes from in vitro aging by reducing oxidative stress and maintaining the mitochondrial functions

Cited by 4 publications

References 37 publications

Mechanisms of mitochondrial dysfunction in ovarian aging and potential interventions

Mechanisms of mitochondrial dysfunction in ovarian aging and potential interventions

Cordycepin delays postovulatory aging of oocytes through inhibition of maternal mRNAs degradation via DCP1A polyadenylation suppression

Protective effect of onion peel extract on ageing mouse oocytes

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