30 SUN CARE


formulation friendly (Figure 2), sustainably manufactured vitamin C derivative which is readily biodegradable. It has been used worldwide in various personal care products since its launch in 1995. Previous studies demonstrated that ascorbyl


glucoside effectively inhibits acute sunburn.3 However, its impact on chronic UV damage - such as wrinkle formation and other signs of photoageing - remains insufficiently explored. In this study, we conducted both in vitro and


in vivo studies to further clarify the effects of ascorbyl glucoside on cumulative sun damage.


Suppression of UVA-induced damage to dermis Solar UV radiation reaching the Earth’s surface contains UV rays of two different wavelengths: UVA (315-400 nm), and UVB (280-315 nm) (Figure 1). UVA is regarded as the predominant factor in photoageing because it can penetrate deeply to the dermis, and contributes to long- term deterioration of dermal structure. In the dermis, fibroblasts produce a collagen-rich extracellular matrix (ECM), which provides mechanical strength and resiliency to the skin.4 UVA radiation causes oxidative stress, which affects both fibroblasts and the ECM.5


In the


previous study, the protective effect of ascorbyl glucoside on fibroblasts against oxidative stress was demonstrated, however protection against UVA had not yet been confirmed.6 To investigate the effect of ascorbyl


glucoside against UVA in the dermis, an in vitro test using NHDF (normal human dermal fibroblasts) was performed. Firstly, cells were incubated for 72 hours


with 0.25 or 1 mmol/L ascorbyl glucoside, and were exposed to 5 J/cm2


UVA radiation


in the presence of riboflavin, which is a photosensitizer to amplify oxidative stress due to UVA.


The decrease of cell viability induced by UVA


was significantly suppressed by pre-treatment with ascorbyl glucoside in a dose dependent manner (Figure 3), which suggests that ascorbyl glucoside reduces oxidative stress due to UVA irradiation, and therefore suppresses cell death. In addition to tests on dermal cells, the


120 100 80 60 40 20 0


Control -UVA


0


effect of ascorbyl glucoside on type I collagen, the major component of ECM, was investigated. When the skin is exposed to UVA, fibrils of


type I collagen undergo oxidative stress due to accumulation of reactive oxygen species (ROS). Among several kinds of ROS, singlet oxygen is known to cause cross-linking of collagen fibres, which critically determines the physical properties of skin. Undesirable cross-linking of collagen fibres is considered to be one of the factors that cause skin ageing.7 To evaluate the effect of ascorbyl glucoside


on collagen cross-linking, the gelation of a collagen solution under UVA irradiation was observed. In this study, a mixture of a 0.2% collagen solution, riboflavin, and 1, 5, or 10 mmol/L ascorbyl glucoside was prepared, and exposed to 2 J/cm2


UVA radiation.


The collagen solution without ascorbyl glucoside transformed to a solid gel due to


cross-linking of collagen fibres. On the other hand, a solution with the addition of ascorbyl glucoside remained liquid (Figure 4), which indicates inhibition of gelation due to UVA. This suggests that ascorbyl glucoside has a protective effect against UVA damage on type- collagen.


Suppression of UVB-induced damage to basement membrane The basement membrane (BM), situated at the dermal-epidermal junction, is essential for maintaining the structural integrity of the skin. It is also responsible for the signs of photoageing, since a BM damaged by UV is considered to alter the structure of the dermis, resulting in skin wrinkling and sagging.8 Type IV collagen is the major component


of the basal lamina, which functions as a backbone of the BM (Figure 5).9


UVB causes


damage to the structure of the BM by inducing the degradation of type IV collagen, facilitating signs of ageing, as well as UVA, the predominant factor in photoageing.10 Several studies have shown that ascorbic


* * *


acid promotes type IV collagen expression and assists BM formation, but similar effects have not been widely reported with ascorbyl glucoside.11,12


In addition, the protective effect


of ascorbyl glucoside against UVB has not been reported yet. Firstly, to investigate the effect of


0.25 + UVA


1


ascorbyl glucoside (mmoI/L


Figure 3: Cell viability in UVA-irradiated NHDF pre-treated, or not pre-treated, with ascorbyl glucoside. N=4, Mean ± SD, *p<0.05 (Tukey-Kramer test in + UVA)


PERSONAL CARE April 2025


ascorbyl glucoside on the structure of the BM, immunostaining of type IV collagen was carried out using a full thickness 3D skin model consisting of NHDF, NHEK (Normal Human Epidermal Keratinocytes), and the stratum corneum. In addition, the amount of type IV collagen was measured from extracts of 3D skin model samples. After 48 hours of incubation, the 3D


skin model treated with 2% ascorbyl glucoside showed a clearer pattern of


www.personalcaremagazine.com 2% ascorbyl glucoside gel (adjusted to pH 6.4)


Residual amount of ascorbyl glucoside (%)


100 80 60 40 20 0


Initial 6 months* Retained 98.5% 40°C / 6 months


* Storage of 6 months at 40°C simulates a 3-year shelf life (at 25°C) based on Arrhenius equation.


Figure 2: Stability of gel formulation containing 2% ascorbyl glucoside 40°C


Cell viability (%) relative to control


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