60 SUN CARE repair systems,6 but they can still be affected
by UVA. Indeed, DNA lesions induced by UVA in
keratinocytes are associated with a weakening of their self-renewal capacity, their so-called ‘stemness’ potential, ultimately related to functional and structural alterations of the epidermis. Out of this collaboration, an all-natural
active ingredient has been developed with the objective to preserve keratinocyte stem cells from UVA-induced damage and ultimately answer to concerns about photoageing and skin health.7
Mechanism of action This ingredient has been specifically selected for its ability to act at the heart of the epidermis mechanics. It enables to protect the epidermal stem cells from UVA-induced DNA damage and to preserve the regeneration capacity of the epidermis. Several in vitro models have been combined to evaluate its broad range of efficacies. The ingredient can act at several stages of
the DNA damage process. At an early stage, the ingredient reduces the oxidative pressure (ROS) inside keratinocytes, which are the first consequence of UVA radiation (-30% in UVA-irradiated keratinocytes as compared to untreated cells). Consequently, it can prevent the formation
of oxidative DNA lesions such as 8-oxoguanine (8-oxoG). 8-oxoG is an oxidative DNA lesion of a guanine base, typical of UVA rays. Its induction has been quantified in a monolayer culture of keratinocytes after UVA exposure through a comet assay. This reference method measures DNA damage in cells. After UVA irradiation, cells undergo a specific
treatment using an enzyme targeting oxidative DNA lesions (Fpg) and electrophoresis to induce DNA migration. The DNA damaged by UVA is separated from the intact (the ‘head’) and generates a comet (the ‘tail’). The longer the comet, the more the DNA is damaged (Figure 1). The treatment with the active decreases by 68% the induction of 8-oxoG in UVA-irradiated keratinocytes as the length of the comet shows, confirming that cells are significantly protected against oxidative DNA lesions. Furthermore, the ingredient demonstrates
capacities to boost the endogenous DNA repair systems linked to different types of lesions.
CONTROL UNTREATED/NO STRESS
70 60 50 40 30 20 10 0
-68%***
No stress Untreated
UV
No stress
UV Solastemis™ 0.5% ***: p<0.001
Figure 1 : Protection against oxidative DNA lesions (8-oxoguanine lesions, measured through a comet assay)
Indeed, using DNA biochips holding three types of DNA lesions (abasic sites, CPD-64, Glycols lesions), an increase of the enzymatic repair activity up to x2.3 has been observed showing a global improvement of the DNA repair pathway. Ultimately, the ingredient was evaluated
in a clonogenic assay to study its protective activity on keratinocyte stem cells exposed to UVA. Keratinocytes treated with the ingredient display an improved self-renewal potential compared to untreated ones. This guarantees the maintenance of the
stemness capacity of keratinocytes, even under sun exposure associated with a preservation of the epidermal homeostasis and health over the long term. Beyond epidermis, the ingredient was
tested on skin biopsies to evaluate its effect on the dermis. It appears as a biological shield for the extra-cellular matrix, protecting the elastic fibers and collagen networks from degradation. The induction of MMP-12, a protease
involved in the degradation of the extra- cellular matrix is reduced under the treated condition, while the elastin and collagen I synthesis are boosted in comparison to the untreated condition, +206% and +191% respectively (Figure 2).
CONTROL UNTREATED/UV
Visible results vs. placebo These in vitro efficacies were confirmed in a double-blind clinical trial, involving 33 Caucasian women (48.5 y.o. on average) with photoaged skin. The panelists applied a cream containing 2% of the active on the half-face, twice daily for 56 days (with an interim evaluation at D28). A placebo cream was applied on the other half-face. A panel of methodologies has been used to assess the active capacity to reduce symptoms associated with sun exposure and photoageing. Results showed a clear anti-wrinkles effect, statistically significant versus the placebo. The image analyses of 3D acquisitions
obtained with the AEVA device revealed an important reduction of the crow’s feet wrinkles: -12.5% in length and area of wrinkles, -12.2% in volume (Figure 3). The skin complexion which tends to become
uneven and dull with overexposure to sun, has also been studied on 2D acquisitions using the ColorFace® device (Figure 4). It revealed an improvement of the skin radiance associated with a global brightening effect (ITA°: +13.3%). These results are associated with a reduction
of the physiological age of the volunteers by 3.6 years on average (0.8 years for the placebo,
SOLASTEMIS™ 0.5% + UV
+191% ****
Figure 2: Collagen I protection against UV radiation Fibrillar organization of type 1 collagen fibers
PERSONAL CARE October 2022 Loss of fibrillar organization Fibrillar organization of type 1 collagen fibers
Collagen I expression vs. Control untreated/UV
**** p<0.0001
www.personalcaremagazine.com
Fpg Sensitive sites (% of tail intensity)
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