Protective effect of pre- and post-vitamin C treatments on UVB-irradiation-induced skin damage

Kawashima, Saki; Funakoshi, Tomoko; Sato, Yasunori; Saito, Norikatsu; Ohsawa, Hajime; Kurita, Katsumi; Nagata, Kisaburo; Yoshida, Masayuki; Ishigami, Akihito

doi:10.1038/s41598-018-34530-4

Cited by 59 publications

(53 citation statements)

References 52 publications

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“…Several studies have reported that ascorbic acid decreases UVB-induced ROS production, and prevents ROS-medicated DNA damage and apoptosis in epidermal keratinocytes [ 48 , 49 ]. Pre- and post-treatment of reconstituted human epidermis with ascorbic acid reduced UVB-induced cell death, apoptosis, DNA damage, ROS production, and the inflammatory response by suppressing tumor necrosis factor-α (TNF-α) production [ 50 ].…”

Section: Antioxidants and Interfollicular Epidermal Stem Cellsmentioning

confidence: 99%

Antioxidants as an Epidermal Stem Cell Activator

Kwon

Park

2020

Antioxidants

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Antioxidants may modulate the microenvironment of epidermal stem cells by reducing the production of reactive oxygen species or by regulating the expression of extracellular matrix protein. The extracellular membrane is an important component of the stem cell niche, and microRNAs regulate extracellular membrane-mediated basal keratinocyte proliferation. In this narrative review, we will discuss several antioxidants such as ascorbic acid, plant extracts, peptides and hyaluronic acid, and their effect on the epidermal stem cell niche and the proliferative potential of interfollicular epidermal stem cells in 3D skin equivalent models.

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Section: Antioxidants and Interfollicular Epidermal Stem Cellsmentioning

confidence: 99%

Antioxidants as an Epidermal Stem Cell Activator

Kwon

Park

2020

Antioxidants

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“…Vitamin C could reduce oxidative stress production and inflammation to achieve protective effects. Researches showed that vitamin C could suppress UVB-induced cell death, apoptosis, ROS production, and the inflammatory response by downregulating tumor necrosis factor-α (TNF-α) expression [14,15]. Moreover, UVB irradiation of vitamin-deficient animals resulted in severe corneal injury and -inflammatory response [16].…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Vitamin C against Infancy Rat Corneal Injury Caused by Acute UVB Irradiation

Chen

Guo

et al. 2020

BioMed Research International

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Purpose. Studies have shown that corneas of young children were more susceptible to Ultraviolet B (UVB) radiation damage. However, there exist limited information about the harm of UVB to eyes and preventive measures on infancy. Vitamin C as an antioxidant is widely used to prevent many diseases. Therefore, the aim of this study was to explore the protective effect of vitamin C on the cornea of infant rats with acute UVB injury. Method. Thirty-six infant rats were randomly divided into three groups: control (CON) group, UVB (UVB) group, and UVB+vitamin C (UVB+VitC) group. The UVB group was exposed to UVB irradiation (8 J/cm2, 15 min/d, 7 d) and the UVB+vitamin C group suffered the same UVB irradiation treated with vitamin C at the dose of 40 mg/kg via intraperitoneal injection. Then, corneal morphology was detected in vivo and in vitro at 7 d post-UVB exposure. Furthermore, serum inflammatory factors (IL-1, IL-6, and TNF-α) and oxidative status (4-HNE and MDA) were detected by ELISA, and the expression of vascular endothelial growth factor-α (VEGF-α) and superoxide dismutase (SOD) in the cornea was detected by western blot or immunofluorescent staining. Results. Slit lamp detection revealed that the area of corneal desquamation and corneal neovascularization in the UVB+VitC group was significantly less than those in the UVB group at 7 d post-UVB exposure (all p<0.05). OCT results showed that the thickness of the central cornea in the UVB+VitC group was decreased than that in the UVB group (p<0.05). The serum inflammatory factors (IL-1, IL-6, and TNF-α) and oxidative status (4-HNE and MDA) in the UVB group were significantly increased compared with the CON group (all p<0.05), while those factors in the UVB+VitC group were decreased compared with those in the UVB group. Furthermore, the expression of VEGF-α in the UVB+VitC group was dramatically decreased compared with that in the UVB group (p<0.05), and the expression of SOD2 in the UVB+VitC group was dramatically increased compared with that in the UVB group at 7 d post-UVB exposure (p<0.05). Conclusion. Vitamin C could protect infant rats from corneal injury induced by UVB via alleviating corneal edema, improving corneal inflammatory reaction, and decreasing VEGF-α expression.

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“…In human skin in vivo and pig skin, the topical application of aqueous solution containing 15% vitamin C and stabilized with 1% vitamin E and 0.5% ferulic acid at low pH (as observed in formulation 1 and 2) reduces UVA radiation–induced erythema 20,22 . In addition, the administration of vitamin C in the medium protects reconstituted human epidermis or keratinocyte 3D cultures against DNA damage, inflammation, and apoptosis induced by UVA and UVB radiation 17,43 . However, some participants have reported redness and burning on their face after application of the anti‐aging moistures with 30% vitamin C 44 .…”

Section: Discussionmentioning

confidence: 99%

“…In the dermis, vitamin C promotes the synthesis of elastic and collagen fibers in humans and rodents 10‐14 . In addition, topical administration of vitamin C protects skin against UV radiation–induced oxidative damage in pig models or reconstituted human epidermis 15‐17 . Nonetheless, the stability of such vitamin C formulations is essential for maximizing the protective effect.…”

Section: Introductionmentioning

confidence: 99%

Topical application of a commercially available formulation of vitamin C stabilized by vitamin E and ferulic acid reduces tissue viability and protein synthesis in ex vivo human normal skin

Romana‐Souza

Silva-Xavier

Monte‐Alto‐Costa

2020

J of Cosmetic Dermatology

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Background Aqueous formulations of vitamin C stabilized by vitamin E and ferulic acid at low pH effectively protect skin against reactive oxygen species‐induced damage. However, the effects of these formulations on human skin have not clearly been described. The aim of this study was to investigate whether topical application of two commercially available formulations of vitamin C alter human skin using an ex vivo model. Methods Human skin explants were topically treated on alternate days with commercially available formulation 1 (15% vitamin C) at 100% (without dilution), 50%, or 10% diluted in saline or formulation 2 (20% vitamin C) at 100% (without dilution), 50%, or 10% diluted in saline. Only saline was applied to control skin explants. Results Topical formulation 1 at 100%, 50%, or 10%, but not formulation 2 at 100%, 50%, or 10%, reduced the viability of ex vivo human skin compared to the control after 7, 10, and 13 days. In addition, compared to the control, ex vivo human skin treated with formulation 1 at 50%, but not formulation 2 at 50%, also decreased mRNA levels of actin and ribosomal protein L10 and gene expression of extracellular matrix components after 10 days. Furthermore, after 10 days, topical application of formulation 1 at 50%, but not formulation 2 at 50%, decreased the protein expression of proliferating cellular nuclear antigen, lysyl oxidase, β‐actin, and glyceraldehyde‐3‐phosphate dehydrogenase compared to the control. Conclusions Topical formulation 1, but not formulation 2, may reduce the viability of and protein synthesis in ex vivo human skin. Those effects might be due to action of vehicle of formulation 1 on ex vivo human skin.

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Protective effect of pre- and post-vitamin C treatments on UVB-irradiation-induced skin damage

Cited by 59 publications

References 52 publications

Antioxidants as an Epidermal Stem Cell Activator

Antioxidants as an Epidermal Stem Cell Activator

Protective Effect of Vitamin C against Infancy Rat Corneal Injury Caused by Acute UVB Irradiation

Topical application of a commercially available formulation of vitamin C stabilized by vitamin E and ferulic acid reduces tissue viability and protein synthesis in ex vivo human normal skin

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