Protective effects of coenzyme Q10 on cell damage induced by hydrogen peroxides in cultured skin fibroblasts
Open accessAbstract
Cellular senescence is an intricate and multifactorial phenomenon, which is characterized by an irreversible cellular growth arrest, it is caused in response to irretrievably DNA damage, telomere shorting, activation of oncogene, and oxidative stress. Human diploid fibroblasts are a well-established experimental model for premature senescence-related studies, and exposure of fibroblasts to H2O2 is widely used as a SIPS model. Recently, it has been reported many studies of CoQ10 as to anti-aging effects, however the effect of CoQ10 on H2O2-induced SIPS model of human skin fibroblasts has not been understood. So that, we investigated that human skin fibroblasts were used to investigate the prevention effect of CoQ10 against H2O2-induced SIPS model. We created SIPS model fibroblasts with treatment of 100 μM H2O2 for 2 h. In this study, CoQ10 also increased cell viability and mRNA levels of type I, IV collagen and protein level of type I collagen. Moreover, it is shown that CoQ10 suppressed oxidative stress, degradation of collagen by increasing MMP expression, and decreasing senescence-associated phenotypes (e.g. SA-βgal positive staining and SASP) for preventing skin aging via H2O2-induced SIPS model. These results suggested that CoQ10 has possibility to be contributory for extension of healthy life expectancy in Japan.
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In vitro studies on human skin fibroblasts exposed to H2O2 have shown that cell treatment with CoQ10 significantly reduced OS, decreased SA-β gal positive cells and restored collagen type I protein and senescence-associated MMP production, therefore delaying skin aging.
“In vitro studies conducted on human skin fibroblasts exposed to H2O2 have shown that cell treatment with CoQ10 significantly reduced OS, decreased the amount of SA-β gal positive cells and restored collagen type I protein and the senescence-associated matrix metalloproteinase (MMP) production, therefore delaying skin aging [63].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [63]
Coenzyme Q10, SkQ1, mitoquinone and methylene blue are among mitochondria targeted antioxidants exerting a role in counteracting OS-induced senescence, with CoQ10 being the most studied.
“Coenzyme Q10 (CoQ10), SkQ1 (a.k.a. visomitin), mitoquinone (MitoQ) and methylene blue are among the mitochondria targeted antioxidants exerting a role in counteracting OS-induced senescence, with CoQ10 being the most studied (Table 1 and Table 2) [57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [63]
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The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence
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- Authors
- Mine, Y., Takahashi, T., & Okamoto, T.
- Affiliations
- Kobe Gakuin University (JP)
- Corresponding author
- Mine, Yukitoshi
- ORCID
- Takahashi, Takayuki
- Venue
- Journal of Clinical Biochemistry and Nutrition
- Published
- 2021
- Volume
- 69
- Issue
- 3
- Pages
- 247-255
- ISSN
- 0912-0009 (ISSN-L)
- 1880-5086
- PMC
- PMC8611366
- OpenAlex
- W3160720955
- Cited by
- 5
- References
- 44
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 1 · 2022: 2
- FWCI
- 0.31
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- cc-by-nc-nd
- Locations
- Journal of Clinical Biochemistry and Nutrition (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- coenzyme Q10, hydrogen peroxide, premature senescence, dermal fibroblasts, cellular senescence, oxidative stress, skin aging, collagen, matrix metalloproteinases, senescence-associated β-galactosidase, senescence-associated secretory phenotype, cell viability
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