Anti-Inflammatory Effect of Ubiquinol-10 on Young and Senescent Endothelial Cells via MiR-146a Modulation
Abstract
Clinical evidence demonstrates that ubiquinol-10, the reduced active form of coenzyme Q10 (CoQ10H₂), improves endothelial function through its antioxidant and probably its anti-inflammatory properties. We previously reported that a biomarker combination including miR-146a, its target protein IL-1 receptor-associated kinase (IRAK-1), and released interleukin (IL)-6, here collectively designated as MIRAKIL, indicates senescence-associated secretory phenotype (SASP) acquisition by primary human umbilical vein endothelial cells (HUVECs). We explore the ability of short- and long-term CoQ10H₂ supplementation to affect MIRAKIL in HUVECs, used as a model of vascular aging, during replicative senescence in the absence/presence of lipopolysaccharide (LPS), a proinflammatory stimulus. Senescent HUVECs had the same ability as young cells to internalize CoQ10 and exhibit an improved oxidative status. LPS-induced NF-κB activation diminished after CoQ10H₂ pretreatment in both young and senescent cells. However, short-term CoQ10H₂ supplementation attenuated LPS-induced MIRAKIL changes in young cells; in senescent cells CoQ10H₂ supplementation significantly attenuated LPS-induced miR-146a and IRAK-1 modulation but failed to curb IL-6 release. Similar results were obtained with long-term CoQ10H₂ incubation. These findings provide new insights into the molecular mechanisms by which CoQ10H₂ stems endothelial cell inflammatory responses and delays SASP acquisition. These phenomena may play a role in preventing the endothelial dysfunction associated with major age-related diseases.
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Diminished inflammation, OS-induced senescence and apoptosis have been observed in HUVEC with CoQ10H2 in other studies.
“Diminished inflammation, OS-induced senescence and apoptosis have also been observed in the same cell line in other studies [69,72].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [69]
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- Authors
- Olivieri, F., Lazzarini, R., Babini, L., Prattichizzo, F., Rippo, M. R., Tiano, L., Di Nuzzo, S., Graciotti, L., Festa, R., Brugè, F., Orlando, P., Silvestri, S., Capri, M., Palma, L., Magnani, M., Franceschi, C., Littarru, G. P., & Procopio, A. D.
- Affiliations
- Marche Polytechnic University (IT)
- University of Bologna (IT)
- University of Urbino (IT)
- Corresponding author
- Olivieri, Fabiola
- ORCID
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2013-10
- Volume
- 63
- Pages
- 410-420
- ISSN
- 0891-5849 (ISSN-L)
- OpenAlex
- W2007573842
- Cited by
- 84
- References
- 48
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 5 · 2023: 3 · 2022: 16 · 2021: 16 · 2020: 10 · 2019: 5 · 2018: 5 · 2017: 5 · 2016: 6 · 2015: 4 · 2014: 2 · 2013: 2
- FWCI
- 2.09
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion)
- Università Politecnica delle Marche (Università Politecnica delle Marche) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- ubiquinol-10, coenzyme Q10, endothelial cell senescence, miR-146a, IRAK1, interleukin-6, senescence-associated secretory phenotype, vascular aging, lipopolysaccharide, NF-κB activation, endothelial inflammation, oxidative status, endothelial dysfunction
- MeSH terms
- Aging, Antioxidants, Humans, Inflammation, Lipopolysaccharides, Ubiquinone, Interleukin-6, NF-kappa B, Cellular Senescence, MicroRNAs, Endothelial Cells, Interleukin-1 Receptor-Associated Kinases, Human Umbilical Vein Endothelial Cells
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