ArticleFrontiers in nutrition2023
Luteolin regulates the distribution and function of organelles by controlling SIRT1 activity during postovulatory oocyte aging.
Article in Frontiers in nutrition, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- From collapse to comeback: Luteolin rejuvenates nucleus pulposus progenitor cells via SIRT1/ATF5-UPRmt to reverse intervertebral disc degeneration cascade.Stem cell research & therapy · 2026Article
- Review
- Network pharmacology and molecular docking to explore the potential mechanism of Codonopsis pilosula delaying aging.Medicine · 2025Article
- Article
- L-Tryptophan Produced by Bifidobacterium pseudocatenulatum NCU-08 Delays Aging in SAMP8 Mice by Activating the Sirt1/P53/P21/Rb Signaling Pathway.Aging cell · 2025Article
- Network pharmacology and molecular docking to elucidate the mechanism of antiaging of Platycodon grandiflorus.Medicine · 2025Article
- Research Progress on the Interaction Between SIRT1 and Mitochondrial Biochemistry in the Aging of the Reproductive System.Biology · 2025Review
- Anti-Graying Effects of External and Internal Treatments with Luteolin on Hair in Model Mice.Antioxidants (Basel, Switzerland) · 2024Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The quality of oocytes determines their development competence, which will be rapidly lost if the oocytes are not fertilized at the proper time after ovulation. SIRT1, one of the sirtuin family members, has been proven to protect the quality of oocytes during postovulatory oocyte aging. However, evidence of the effect of SIRT1 on the activity of organelles including the mitochondria, the endoplasmic reticulum (ER), the Golgi apparatus, and the lysosomes in postovulatory aging oocyte is lacking. In this study, we investigated the distribution and function of organelles in postovulatory aged oocytes and discovered abnormalities. Luteolin, which is a natural flavonoid contained in vegetables and fruits, is an activator of SIRT1. When the oocytes were treated with luteolin, the abnormal distribution of mitochondria, ER, and Golgi complex were restored during postovulatory oocyte aging. The ER stress protein GRP78 and the lysosome protein LAMP1 increased, while the mitochondrial membrane potential and the Golgi complex protein GOLPH3 decreased in aged oocytes, and these were restored by luteolin treatment. EX-527, an inhibitor of SIRT1, disrupted the luteolin-mediated normal distribution and function of mitochondria, ER, Golgi apparatus, and lysosomes. In conclusion, we demonstrate that luteolin regulates the distribution and function of mitochondria, ER, Golgi apparatus, and lysosomes during postovulatory oocyte aging by activating SIRT1.
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