Free home delivery when you spend £10 or more
VINOPERFECT
Scientific Dossier
SCIENTIFIC CONCEPT
Vinoperfect cosmetic line is intended for people wanting to fight against dark spots and dull complexion.
Skin pigmentation is the result of the production of melanin. This pigment is synthesized in the epidermis by melanocytes and transferred to keratinocytes. In the epidermis, the repartition of melanocytes and melanin is uniform, leading to homogeneous skin color.
This natural skin pigmentation depends on the individual genetics, mostly due to ethnicity, and is a well-regulated mechanism. However, associated to ultraviolet radiations or pollution exposure, factors such as inflammation, aging, hormones can alter the melanogenesis process. As a result, there is an excess of melanin in the epidermis, causing the formation of dark spots.
Caudalie has used its stabilized Viniferin (Patent N°FR21/08421) to regulate the pigmentation process and limit the overproduction of melanin. Associated with White Peony root extract and Niacinamide, it acts on every step of the formation of dark spots. To complete the lightening activity, the exfoliating ingredients increase cell renewal, which helps removal of dark spots as well as boosts radiance.
Thanks to this association of ingredients, the new Vinoperfect collection is efficient against dark spots and hyperpigmentation, and boosts skin radiance.
Table of content
PROBLEM
What causes skin hyperpigmentation and dark spots?
Skin pigmentation is the result of the production of melanin, synthesized by melanocytes and transferred to keratinocytes. Associated to ultraviolet radiations or pollution exposure, factors such as inflammation, aging and hormones can alter the melanogenesis process. As a result, there is an excess of melanin in the epidermis, causing the formation of dark spots.
Skin's natural pigmentation
Skin color results from the presence of a pigment, melanin, in the epidermis. There are two types of melanin: eumelanin, a black-brown pigment, and pheomelanin, a yellow-orange pigment [1]. Skin pigmentation depends on the amount of total melanin, but mostly on the amount of eumelanin [2]. Thus, dark skins contain more melanin than fair skins, but also more eumelanin [3].
Natural skin color is regulated by genetic factors. Thus, from birth, every human being has a different pigmentation, often linked to ethnicity [4]. The various pigmentation types are classified according to the Fitzpatrick system [5]. The classification categorizes 6 different phototypes (Figure 1), depending on the amount of melanin, the skin's reaction to sun exposure and the risk of cancer. Indeed, melanin's main role is to protect cell nuclei from DNA damages caused by ultraviolet radiations.
Figure 1: Fitzpatrick classification. Six skin phototypes have been determined according to melanin amount, UV sensitivity and skin cancer risk. [6].
Process of melanin synthesis
The synthesis of both types of melanin occurs inside melanocytes (Figure 2). These cells contain organelles called melanosomes [7], which are the place of melanin synthesis, storage, and transport [8].
 "Cross-section diagram of skin layers")
Figure 2: The epidermal melanin unit. Melanin is synthesized in melanocytes inside melanosomes. Once melanosomes are filled with melanin, they are transferred to neighboring keratinocytes [9].
Melanin is produced through a series of chemical reaction (Figure 3). The first two steps are catalyzed by the enzyme Tyrosinase and are critical to the process of melanin synthesis. Tyrosinase is involved in the synthesis of both eumelanin and pheomelanin. Two other enzymes are implicated in melanin synthesis: the Tyrosinase-Related Proteins 1 and 2 (TRP-1 and TRP-2). They only participate in the synthesis of eumelanin [10,11].
Figure 3: Reaction of synthesis of eumelanin and pheomelanin [12].
Once charged in melanin, melanosomes are transferred to neighboring keratinocytes. One melanocyte transfers its melanosomes to 36 keratinocytes, on average [13]. Once inside the keratinocytes, melanosomes are found above the nucleus to protect it from UV-induced damage. In dark skins, melanosomes occupy more space than in fair skins, which results in a better natural photoprotection.
Finally, in the course of epidermis renewal, melanosomes are degraded. The degradation happens sooner in fair skins than in dark skins.
Regulation of melanin synthesis
Skin pigmentation is regulated by various factors and biological pathways. Among them, the MITF (Microphtalmia-associated transcription factor) protein plays a crucial role. It regulates the expression of genes implicated in various aspects of the melanogenesis pathway [14]:
• Melanocyte proliferation
• Melanosome formation (Pmel17, MART-1)
• Melanin synthesis (Tyrosinase, TRP-1 and TRP-2)
• Melanin transport to keratinocytes.
The expression of MITF is itself regulated by the activation of a receptor located at the surface of melanocytes: MC1R (Melanocortin 1 Receptor). It is activated by two hormones: α-Melanocyte Stimulating Hormone (α-MSH) and Adrenocorticotropic hormone (ACTH), derived from a precursor called Proopiomelanocortin (POMC), produced by keratinocytes and melanocytes.
Multiple other factors are involved in the regulation of melanin synthesis. Notably, various studies have demonstrated the link between inflammation and pigmentation. Indeed, factors such as prostaglandins, cytokines and interleukins can modulate skin pigmentation [15-17]. Finally, hormonal regulation of skin pigmentation has also been highlighted by some research. For example, estrogen seems to increase melanin synthesis in melanocytes while progesterone seems to decrease it [18,19]. All these mechanisms of regulation are influenced internally, but also by environmental factors.
Acquired pigmentation — Role of ultraviolet radiations
The skin's natural color can be affected by external factors. Among them, exposure to ultraviolet (UV) radiations constitutes the main factor influencing skin pigmentation. Ultraviolet radiations are of three types (Figure 4) [20]:
• UVA (between 320 and 400 nm), penetrate the skin until the deep dermis,
• UVB (between 280 and 320 nm), are mainly absorbed by the epidermis and the superficial dermis,
• UVC (between 100 and 280 nm), are stopped by the ozone layer and generally do not reach the Earth's surface.
Figure 4: Penetration of ultraviolet radiations inside the skin [21].
UV exposure induces a natural response, tanning, which is composed of two phenomena: immediate tanning and delayed tanning. Immediate tanning is mostly provoked by UVA. It appears a few minutes after sun exposure and lasts only a few hours [22]. It is the result of melanin oxidation and melanosome redistribution in the epidermis [23]. Delayed tanning is mainly induced by UVB. It appears 2 to 3 days after sun exposure and is highest after three weeks. The skin's natural color returns 8 to 10 months after exposure [22]. Delayed tanning is the result of the synthesis of new melanin. It also stimulates melanocytes proliferation and activity.
Role of other environmental factors
In addition to UV, other environmental factors modulate skin pigmentation. Studies have demonstrated the role of pollutants, such as particulate matters and tobacco smoke, in hyperpigmentation. Indeed, they increase the expression of Tyrosinase, via the activation of a receptor called AhR (aryl hydrocarbon receptor) [18,24-26].
Skin hyperpigmentations
The mechanisms of skin pigmentation can be altered and lead to an excess of melanin synthesis or transfer. As a result, dark spots can appear at the skin surface. These are of various forms and can be linked to aging, inflammation, or hormonal variations. Nowadays, skin hyperpigmentation constitutes one of the most common causes of dermatologists' consultations, regardless of age, skin color and gender [27].
Melasma
Melasma is characterized by hyperpigmented spots of irregular color (grey to dark brown), localized in sun-exposed areas and mainly in the face (Figure 5).
Figure 5: Moderate melasma on a woman of phototype V [27].
It is promoted by several parameters: genetic predisposition and female sex hormonal modifications (contraception, hormone replacement therapy or pregnancy) [28]. Also, UV exposure an aggravating factor and sometimes a trigger. Women are mostly affected, as well as darker skin phototypes (IV to VI). Melasma is due to an increase in melanocytes size and an overproduction of melanin and melanosome. Studies have shown a stimulation of genes implicated in melanogenesis pathway [29].
Solar lentigo
Solar lentigo (also called age spots, actinic lentigo or senile lentigo) is characterized by light yellow to dark spots of variable size (Figure 6). The appearance of these spots is linked to photoaging: they appear in middle- or advanced-aged individuals, in areas frequently exposed to sun. Caucasian and Asian skins are the most affected (phototypes II to IV) [30].
Figure 6: Solar lentigos [31].
The number of melanocytes in unchanged. However, their activity is greatly stimulated. Studies have shown that various factors involved in the regulation of skin pigmentation are overexpressed, leading to an increase in melanin synthesis and its accumulation in the epidermis [32].
Postinflammatory hyperpigmentation
Postinflammatory hyperpigmentation is characterized by irregular spots appearing further to cutaneous inflammations such as acne, infections, or allergic reactions (Figure 7). They can persist for months or even years after the inflammation. UV is an aggravating factor.
Figure 7: Postinflammatory hyperpigmentation. Dark spots appeared after acne [33].
Postinflammatory hyperpigmentation can affect all skin types but occur mainly in dark phototypes (III to VI). They are linked to an increase in melanin production and transfer in response to inflammation. The excess of melanin can be located in the epidermis (the spot will be brown/dark) or in the dermis (the stain will be grey/blue).
ACTIVE
What is Viniferin and where does it come from?
Viniferin (Patent N°FR21/08421) is a natural polyphenolic antioxidant produced by plants in response to injury or when the plant is under attack by pathogens, such as bacteria or fungi. One of the most common botanical sources is vine; more specifically, vine sap is particularly rich in Viniferin.
Caudalie's stabilized Viniferin was added to the Vinoperfect collection. This ingredient possesses anti-pigmentation effect, that has been demonstrated by various biological tests.
What other lightening ingredients complete Viniferin's activity?
To complete Viniferin's activity, Caudalie has added two other lightening ingredients to some products of the Vinoperfect collection.
White Peony extract
Present in: Brightening Micropeel Foam / Dark Spot Niacinamide Moisturizer / Concentrated Brightening Glycolic Essence / Glycolic Peel Mask.
White Peony extract comes from the roots of an herbaceous plant. Active molecules are mainly represented by paeoniflorin.
It is antioxidant and helps stimulate skin microcirculation [35]. Furthermore, it reduces melanin synthesis in melanocytes by 94%, despite stimulation of melanogenesis (Figure 17).
Figure 8: Effect of White Peony extract on the synthesis of melanin. Normal human melanocytes were stimulated with 1mM L-Tyrosine and 100nM α-MSH, 2 stimulators of melanogenesis, with or without 0.1% White Peony extract. 3 stimulations were done and cells were treated for a total of 7 days. Intracellular melanin content was quantified. A statistical t-test was performed on experimental replicates (n=6).
As a result, clinical tests showed that the use of White Peony extract evens skin tone by reducing redness and dark spots. It also brings radiance to the skin [35].
α-Bisabolol
Present in: Dark Spot Correcting Hand Cream / Dark Spot Correcting Glycolic Night Cream / Radiance Dark Spot Serum / Dark Spot Niacinamide Moisturizer / Glycolic Peel Mask.
α-Bisabolol comes from the essential oil of Candeia tree's bark. It has an inhibiting effect on MITF, Tyrosinase and TRP-1 expression and therefore it reduces melanin content [36] and has a lightening effect [37]. It also demonstrated a soothing effect on volunteers after 4 weeks of treatment [38].
Niacinamide
Present in: Brightening Eye Cream / Dark Spot Niacinamide Moisturizer.
Niacinamide, also known as Vitamin B3, is a synthetic non-irritant molecule. Its ability to inhibit melanin transfer has been demonstrated. Indeed, melanosome transfer is reduced by 68% after 7 days in a melanocyte/keratinocyte coculture treated with Niacinamide [39]. As a result, Niacinamide reduces dark spots and evens skin tone.
Which exfoliating ingredients boost cell renewal and radiance?
In addition to the ingredients acting on hyperpigmentation, Caudalie has added exfoliating ingredients to some products of the Vinoperfect collection.
Glycolic Acid
Present in: Dark Spot Correcting Glycolic Night Cream / Concentrated Brightening Glycolic Essence / Glycolic Peel Mask.
Glycolic acid is an alpha-hydroxy acid (AHA) that gently exfoliates skin and thus enhances cell renewal. In the Vinoperfect collection, Caudalie uses a complex associating glycolic acid with arginine. Indeed, arginine allows an extended liberation of glycolic acid, which significantly decreases skin irritation compared to AHA used alone [40].
Alpha Hydroxy Acids Plant complex
Present in: Glycolic Peel Mask.
This complex of AHA is composed of lactic acid, tartaric acid and citric acid from plant origins. They exfoliate skin and increase cell renewal for a purifying, lightening and smoothing effect.
Papaya extract
Present in: Glycolic Peel Mask / Dark Spot Correcting Glycolic Night Cream / Brightening Micropeel Foam.
Papaya extract contains a keratolytic enzyme called papain. It helps to remove dead cells from skin surface, which brings radiance to the skin [41].
Exfoliating grapefruit extract
Present in: Brightening Micropeel Foam.
Grapefruit extract contains exfoliating fruit acids. It stimulates cell renewal for improved radiance and decreased rugosity [42].
Mandelic acid
Present in: Brightening Micropeel Foam.
Mandelic acid is a synthetic alpha hydroxy acid with keratolytic activity. It is milder than glycolic acid because of its bigger size. Indeed, skin penetration will be reduced.
MECHANISM
How does Viniferin act on dark spots?
To fight against dark spots, Caudalie has chosen ingredients able to counteract all steps of the formation of dark spots (Figure 8). Viniferin acts on hyperpigmentation via three actions on the mechanism of skin pigmentation:
• It reduces the expression of key actors in the pigmentation process, such as Tyrosinase.
• It regulates Tyrosinase activity.
• It inhibits melanin transfer from melanocytes to keratinocytes.
Other known lightening ingredients (Niacinamide and White Peony) have been added to complete Viniferin's activity. Additionally, several exfoliating ingredients have been included in some products. They increase cell renewal on the dark spot site to help its removal. They also boost skin radiance.
Figure 9: Mechanism of action of the ingredients of Vinoperfect on dark spot inhibition.
Thanks to this association of ingredients, the new Vinoperfect collection is efficient against dark spots and hyperpigmentation, and boosts skin radiance.
PROOF
What biological tests prove Viniferin's anti-pigmentation effect?
Inhibition of Tyrosinase activity
Tyrosinase being the most important actor in melanin synthesis, the effect of Viniferin on Tyrosinase activity was studied [34]. It has been shown that Viniferin inhibits Tyrosinase activity. This inhibiting effect is 4 times higher than kojic acid's effect and 62 times higher than ascorbic acid's (Table 1).
IC50 (µM) | Activity ratio against ε-viniferin | |
ε-viniferin | 4.1 ± 0.5 | 1 |
Kojic acid | 16.9 ± 1.1 | 1/4.1 |
Ascorbic acid | 255 ± 10 | 1/62.2 |
Table 1. Inhibition of tyrosinase activity by Viniferin, Kojic acid and Ascorbic acid. Each value of IC50 represents the mean ± SD of three experiments. The effect of ε-viniferin extracted from vine sap on tyrosinase activity was evaluated in tubo using mushroom tyrosinase. For this, the substrate (L-DOPA) was used in presence of the enzyme and different concentrations of tested inhibitors (ε-viniferin, kojic acid and ascorbic acid). Concentration of tested compounds causing 50% inhibition of tyrosinase activity (IC50) are presented in the table.
Inhibition of key pigmentation genes expression
To further demonstrate the anti-hyperpigmentation effect of Viniferin, the expression of various key genes involved in melanin synthesis has been assessed. To do so, skin explants were exposed to pollution particles to induce hyperpigmentation and were treated with a dose equivalent to Vinoperfect Serum. Gene expression was evaluated after 9 days.
Tyrosinase, TRP-1 and TRP-2 enzymes — Caudalie's Viniferin extract protected melanocytes from an increase in Tyrosinase expression due to pollution, and this by 80% (Figure 9). Viniferin also decreased gene expression of the two other enzymes producing melanin, TRP-1 and TRP-2, by 113% and 94%, respectively.
Figure 10: Effect of Viniferin on the gene expression of Tyrosinase. Human skin explants were treated with an emulsion containing 1000 ppm ε-viniferin or its vehicle 2h before topical exposure to pollution particles. After 9 days, gene expression of Tyrosinase was assessed by real-time quantitative PCR and normalized to housekeeping gene 18S rRNA. Fold changes are expressed as mean ± SE (n=3) and a statistical ANOVA SNK test was performed.
The regulator MITF — Caudalie's Viniferin extract protected melanocytes from a pollution-induced increase in MITF expression by 140% (Figure 10).
Figure 11: Effect of Viniferin on the gene expression of MITF. Human skin explants were treated topically with an emulsion containing 1000 ppm ε-viniferin or its vehicle 2h before topical exposure to pollution particles. After 9 days, gene expression of MITF was assessed by real-time quantitative PCR and normalized to housekeeping gene 18S rRNA. Fold changes are expressed as mean ± SE (n=3) and a statistical ANOVA SNK test was performed.
Other key genes — Finally, Caudalie's Viniferin extract limited the overexpression due to pollution of various other key genes involved in the regulation of melanogenesis, but also in the formation of melanosomes (Figure 11).
Figure 12: Effect of Viniferin on the expression of several melanogenesis-associated genes. Human skin explants were treated topically with an emulsion containing 1000 ppm ε-viniferin or its vehicle 2h before topical exposure to pollution particles. After 6 to 9 days, gene expression was assessed by real-time quantitative PCR and normalized to housekeeping gene 18S rRNA. Fold changes are expressed as mean ± SE (n=3) and a statistical ANOVA SNK test was performed.
Reduction of melanin content
Further to the demonstration of Viniferin's ability to inhibit the expression and activity of the pigmentation pathway, its effect on the amount of melanin synthesized in melanocytes was evaluated. Viniferin reduced by 63% the amount of melanin induced by a pro-pigmenting treatment (Figure 12).
Figure 13: Effect of Viniferin on the synthesis of melanin. Human epidermal melanocytes (Caucasian donor) were stimulated with 1mM L-Tyrosine, a stimulator of melanogenesis, with or without 3µg/mL ε-viniferin. 3 stimulations were done, and cells were treated for a total of 10 days. Intracellular melanin content was quantified. A statistical student test was performed on experimental replicates.
Inhibition of melanin transfer
To complete the results obtained on the inhibition of melanin synthesis, the effect of Viniferin on the mechanism of melanin transfer to keratinocytes was evaluated. To do this, human melanocytes and keratinocytes were cultured together and exposed or not to pro-pigmenting factors in order to stimulate the melanosome transfer of melanosomes (containing melanin) from melanocytes to keratinocytes. These cocultures were treated with Viniferin for 3 days. Evaluation of melanosome transfer from melanocytes to keratinocytes was carried out by flow cytometry. Viniferin reduces the number of melanosomes transferred from melanocytes to keratinocytes by 47% (Figure 13). It therefore has a significant inhibitory effect on melanin transfer.
Figure 14: Effect of Viniferin on the transfer of melanin to keratinocytes. Human primary keratinocytes and melanocytes are co-cultured in the presence of pro-pigmenting factors (except for the non-stimulated condition) and treated or not with ε-viniferin for 72 hours. The cells are recovered, labeled with two antibodies and analyzed by flow cytometry. Keratinocytes containing melanosomes are quantified. A Student's statistical test is performed.
Effect on melanin amount in the upper epidermis
To further study melanin transfer, we assessed if Viniferin, at the concentration used in Vinoperfect Serum, can reduce the amount of melanin in the upper epidermis, after UV stimulation. To do so, human skin explants were exposed every day for 3 days to UV and were treated or not by Caudalie Viniferin or Niacinamide. On the fourth day, explants were collected. Fontana-Masson staining and nuclei staining were performed. Image analysis was performed on the upper epidermis to quantify the amount of melanin, normalized by the number of nuclei.
Figure 15: Melanin amount in the upper epidermis of skin explants, irradiated or not by UV, treated or not by Viniferin or Niacinamide. Explants are irradiated every day for 3 days and treated after each irradiation. Results are presented as mean +/- SEM of one experiment performed on 3 explants. The amount of melanin is normalized by the number of nuclei in the epidermis.
In irradiated skin explants, Caudalie Viniferin significantly decreases melanin amount induced by UV irradiation, by 42%. Thus, Viniferin can inhibit melanin transfer to keratinocytes. Viniferin's effect is 43% higher than 10% Niacinamide's in this experiment.
Decrease of skin darkening
Finally, after validating Viniferin's inhibiting effect on melanin synthesis, the outcome of skin coloration was assessed on skin explants, after stimulation of hyperpigmentation by pollution particles. Viniferin significantly improved skin darkening induced by pollution. Indeed, skin was significantly lightened by 42% after 9 days of treatment by 1000ppm of ε-Viniferin (Figure 15).
Figure 16: Effect of Viniferin on skin darkening. Human skin explants were treated topically with an emulsion containing 1000 ppm of ε-viniferin or its vehicle 2h before topical exposure to pollution particles. Skin color was evaluated at day 9 using a colorimeter. A statistical ANOVA SNK test was performed (n=3).
Effect on blue light-induced hyperpigmentation
Blue light, also known as high-energy visible (HEV) light, is part of the visible light spectrum and corresponds to wavelengths between 400 and 500 nm. It is emitted by the sun, but also by artificial light sources (LED bulbs, screens) and penetrates deeper into the skin than UVA rays. Several studies have demonstrated the harmful effects of blue light on the skin. More specifically, it has been shown that blue light causes hyperpigmentation, which is more pronounced than that caused by UV rays and lasts longer.
To continue its studies, Caudalie wanted to determine whether Viniferin, at the concentrations present in creams and in the Vinoperfect serum, was able to inhibit blue light-induced pigmentation in human skin explants.
To do this, human skin explants were irradiated every day for 3 days with blue light at either 412 nm (representative of solar radiation) or 450 nm (representative of light emitted by screens). They were treated or not with Caudalie's stabilized Viniferin at 500 or 1000 ppm, for the duration of the experiment. The amount of melanin present in the explants was measured at the end of the culture. Caudalie's stabilized Viniferin, at the concentrations of Vinoperfect creams and serum, has a significant inhibitory effect on the synthesis of melanin induced by blue light (Figure 16) at two wavelengths, characteristic of solar radiation (412 nm) and screen emission (450 nm).
Figure 17: Melanin content in human skin explants exposed or not exposed to blue light irradiation at 450 nm or 412 nm for three consecutive days, and treated or not treated with Caudalie Viniferine at 500 or 1000 ppm. Explants were treated after each irradiation session. Melanin was solubilized using sodium hydroxide, and melanin content was quantified by measuring absorbance at 405 nm, which is proportional to melanin concentration. The effect of the compounds on pigmentation was calculated relative to the difference between the untreated, non-irradiated control and the corresponding treated conditions.
RESULT
What clinical results does the Vinoperfect collection deliver on consumers?
In addition to the various tests done on the ingredients, efficacy tests were performed on the whole Vinoperfect collection. Indeed, satisfactory tests were realized as well as instrumental clinical tests.
Satisfactory tests — After applying the Radiance Dark Spot Serum twice a day for 56 days, 95% of volunteers found their dark spots were corrected. 97% thought their skin complexion was more even.
65 women of all phototypes, 56 days.
Clinical tests — Clinical tests demonstrated that the Radiance Dark Spot Serum decreased the dark spot's size and color as soon as 7 days of use. After 56 days of use, the dark spot coloration decreased by 63%. On darker skins only, dark spot coloration was reduced by 81%.
Clinical scoring, 65 women of all phototypes (7 and 56 days); darker skins: 33 women of phototypes IV, V, VI, 56 days. Dermscan #20E0949.
Satisfactory tests — After applying the Concentrated Brightening Glycolic Essence twice a day for 56 days, 100% of volunteers found their skin texture was refined and 97% their pores were tightened.
31 women, 56 days.
Clinical tests — Used in association, the Radiance Dark Spot Serum and the Concentrated Brightening Glycolic Essence lightened the skin twice as efficiently as the Serum alone.
Colorimetry, 33 women, 56 days.
Satisfactory tests — After applying the Dark Spot Niacinamide Moisturizer, 95% of volunteers found their skin showed instantly a healthy glow.
20 women, immediate results.
Clinical tests — Instrumental tests showed that the Dark Spot Niacinamide Moisturizer improved skin radiance after 56 days and prevented dark spots appearance.
Chromametry, 20 women, 84 days; VISIA skin imaging analysis, 20 women, 84 days.
Satisfactory tests — After applying the Dark Spot Correcting Glycolic Night Cream daily for 56 days, 93% of volunteers found their skin was more radiant. 80% of them felt their dark spots were lighter.
39 women, 56 days.
Clinical tests — Instrumental tests showed that applying the Dark Spot Correcting Glycolic Night Cream significantly decreased dark spot coloration and size after 56 days. After 56 days, volunteers noticed dark spot intensity reduce by 25%.
ITA + dark spot surface and diameter measurements, 39 women, 56 days; self-scoring, 40 women, 56 days .
Satisfactory tests — After applying the Glycolic Peel Mask twice a week for 28 days, 100% of volunteers found their complexion was less dull and more radiant. All of them thought the mask gave their skin an instant and lasting radiance boost.
19 women, 28 days.
Clinical tests — Instrumental tests showed that the Glycolic Peel Mask improved instantly skin brightness by 33%. Furthermore, the mask demonstrated a smoothing effect on skin texture.
Clinical scoring, 23 women, immediate results (brightness); clinical scoring, 19 women, 28 days (texture).
Satisfactory tests — After applying the Dark Spot Correcting Hand Cream daily for 56 days, 85% of volunteers found their skin was brighter and 83% thought their skin was more even. 93% of volunteers felt their skin nourished.
41 women, 56 days.
Clinical tests — Instrumental tests showed that the Dark Spot Correcting Hand Cream significantly decreased dark spot pigmentation after 56 days of use.
Colorimetry, 41 women, 56 days.
Satisfactory tests — After applying the Brightening Eye Cream daily for 56 days, 86% of volunteers found their dark circles were lightened and 82% thought they were reduced. 95% of volunteers felt the ceramic tip placed in the fridge had a decongesting effect.
22 women, 56 days.
Clinical tests — Instrumental tests showed that the Brightening Eye Cream had a significant decongesting effect on dark circles as soon as the first application.
Laser Doppler, 12 women, 1 day.
Satisfactory tests — 30 seconds after applying the Brightening Micropeel Foam, 81% of volunteers felt a new skin effect and 86% thought their complexion was brighter.
21 women, 1 day.
Clinical tests — Instrumental tests showed that used together, the Brightening Micropeel Foam and the Radiance Dark Spot Serum had a significant stimulating effect on cell renewal. Clinical scoring revealed that the two products used together significantly increased radiance (+22%) and complexion uniformity after 28 days of use.
DHA method, 20 women, 10 days; Clinical scoring, 33 women, 28 days.
All these results support the clinical beneficial effects of the Vinoperfect collection to fight against dark spots and dull complexion.
REFERENCES
[1] Ito, S., and Wakamatsu, K., 2008, "Chemistry of Mixed Melanogenesis--Pivotal Roles of Dopaquinone," Photochem Photobiol, 84(3), pp. 582-592. https://doi.org/10.1111/j.1751-1097.2007.00238.x.
[2] Del Bino, S., Ito, S., Sok, J., Nakanishi, Y., Bastien, P., Wakamatsu, K., and Bernerd, F., 2015, "Chemical Analysis of Constitutive Pigmentation of Human Epidermis Reveals Constant Eumelanin to Pheomelanin Ratio," Pigment Cell Melanoma Res, 28(6), pp. 707-717. https://doi.org/10.1111/pcmr.12410.
[3] Thody, A. J., Higgins, E. M., Wakamatsu, K., Ito, S., Burchill, S. A., and Marks, J. M., 1991, "Pheomelanin as Well as Eumelanin Is Present in Human Epidermis," J Invest Dermatol, 97(2), pp. 340-344. https://doi.org/10.1111/1523-1747.ep12480680.
[4] Sturm, R. A., Box, N. F., and Ramsay, M., 1998, "Human Pigmentation Genetics: The Difference Is Only Skin Deep," Bioessays, 20(9), pp. 712-721. https://doi.org/10.1002/(SICI)1521-1878(199809)20:9<712::AID-BIES4>3.0.CO;2-I.
[5] Fitzpatrick, T. B., 1988, "The Validity and Practicality of Sun-Reactive Skin Types I through VI," Arch Dermatol, 124(6), pp. 869-871. https://doi.org/10.1001/archderm.124.6.869.
[6] D'Orazio, J., Jarrett, S., Amaro-Ortiz, A., and Scott, T., 2013, "UV Radiation and the Skin," Int J Mol Sci, 14(6), pp. 12222-12248. https://doi.org/10.3390/ijms140612222.
[7] Seiji, M., Shimao, K., Birbeck, M. S., and Fitzpatrick, T. B., 1963, "Subcellular Localization of Melanin Biosynthesis," Ann N Y Acad Sci, 100, pp. 497-533.
[8] Delevoye, C., Giordano, F., van Niel, G., and Raposo, G., 2011, "La Biogenèse Des Mélanosomes," Med Sci (Paris), 27(2), pp. 153-162. https://doi.org/10.1051/medsci/2011272153.
[9] "Pigmentation | Biology for Majors II," Lumen Learning. [Online]. Available: https://courses.lumenlearning.com/wm-biology2/chapter/pigmentation/. [Accessed: 07-Feb-2021].
[10] Passeron, T., Ballotti, R., and Ortonne, J.-P., 2005, "Mélanogenèse," EMC - Dermatologie-Cosmétologie, 2(4), pp. 204-216. https://doi.org/10.1016/j.emcdc.2005.10.001.
[11] Tsukamoto, K., Jackson, I. J., Urabe, K., Montague, P. M., and Hearing, V. J., 1992, "A Second Tyrosinase-Related Protein, TRP-2, Is a Melanogenic Enzyme Termed DOPAchrome Tautomerase," EMBO J, 11(2), pp. 519-526.
[12] Hassanaly, S., 2017, "Modulation de La Pigmentation En Conditions de Physioxie: Effet de Nouveaux Phosphosaccharides," These de doctorat, Orléans. [Online]. Available: http://www.theses.fr/2017ORLE2017. [Accessed: 08-Feb-2021].
[13] Boissy, R. E., 2003, "Melanosome Transfer to and Translocation in the Keratinocyte," Exp Dermatol, 12 Suppl 2, pp. 5-12. https://doi.org/10.1034/j.1600-0625.12.s2.1.x.
[14] Cheli, Y., Ohanna, M., Ballotti, R., and Bertolotto, C., 2010, "Fifteen-Year Quest for Microphthalmia-Associated Transcription Factor Target Genes," Pigment Cell Melanoma Res, 23(1), pp. 27-40. https://doi.org/10.1111/j.1755-148X.2009.00653.x.
[15] Scott, G., Leopardi, S., Printup, S., Malhi, N., Seiberg, M., and Lapoint, R., 2004, "Proteinase-Activated Receptor-2 Stimulates Prostaglandin Production in Keratinocytes: Analysis of Prostaglandin Receptors on Human Melanocytes and Effects of PGE2 and PGF2alpha on Melanocyte Dendricity," J Invest Dermatol, 122(5), pp. 1214-1224. https://doi.org/10.1111/j.0022-202X.2004.22516.x.
[16] Yamaguchi, Y., and Hearing, V. J., 2009, "Physiological Factors That Regulate Skin Pigmentation," Biofactors, 35(2), pp. 193-199. https://doi.org/10.1002/biof.29.
[17] Fu, C., Chen, J., Lu, J., Yi, L., Tong, X., Kang, L., Pei, S., Ouyang, Y., Jiang, L., Ding, Y., Zhao, X., Li, S., Yang, Y., Huang, J., and Zeng, Q., 2020, "Roles of Inflammation Factors in Melanogenesis (Review)," Mol Med Rep, 21(3), pp. 1421-1430. https://doi.org/10.3892/mmr.2020.10950.
[18] El-Domyati, M., Attia, S., Saleh, F., Brown, D., Birk, D. E., Gasparro, F., Ahmad, H., and Uitto, J., 2002, "Intrinsic Aging vs. Photoaging: A Comparative Histopathological, Immunohistochemical, and Ultrastructural Study of Skin," Exp. Dermatol., 11(5), pp. 398-405. https://doi.org/10.1034/j.1600-0625.2002.110502.x.
[19] Cario, M., 2019, "How Hormones May Modulate Human Skin Pigmentation in Melasma: An in Vitro Perspective," Exp Dermatol, 28(6), pp. 709-718. https://doi.org/10.1111/exd.13915.
[20] Stanojevi, M., Stanojevi, Z., Jovanovic, D., and Stojiljkovi, M., 2004, "Ultraviolet Radiation and Melanogenesis," Archive of Oncology, 12, pp. 203-205. https://doi.org/10.2298/AOO0404203S.
[21] Pérez-Sánchez, A., Barrajón-Catalán, E., Herranz-López, M., and Micol, V., 2018, "Nutraceuticals for Skin Care: A Comprehensive Review of Human Clinical Studies," Nutrients, 10(4). https://doi.org/10.3390/nu10040403.
[22] Tadokoro, T., Yamaguchi, Y., Batzer, J., Coelho, S. G., Zmudzka, B. Z., Miller, S. A., Wolber, R., Beer, J. Z., and Hearing, V. J., 2005, "Mechanisms of Skin Tanning in Different Racial/Ethnic Groups in Response to Ultraviolet Radiation," J Invest Dermatol, 124(6), pp. 1326-1332. https://doi.org/10.1111/j.0022-202X.2005.23760.x.
[23] Gilchrest, B. A., Park, H. Y., Eller, M. S., and Yaar, M., 1996, "Mechanisms of Ultraviolet Light-Induced Pigmentation," Photochem Photobiol, 63(1), pp. 1-10. https://doi.org/10.1111/j.1751-1097.1996.tb02988.x.
[24] Peng, F., Tsuji, G., Zhang, J.-Z., Chen, Z., and Furue, M., 2019, "Potential Role of PM2.5 in Melanogenesis," Environ Int, 132, p. 105063. https://doi.org/10.1016/j.envint.2019.105063.
[25] Suo, D., Zeng, S., Zhang, J., Meng, L., and Weng, L., 2020, "PM2.5 Induces Apoptosis, Oxidative Stress Injury and Melanin Metabolic Disorder in Human Melanocytes," Experimental and Therapeutic Medicine, 19(5), pp. 3227-3238. https://doi.org/10.3892/etm.2020.8590.
[26] Furue, M., and Tsuji, G., 2019, "Chloracne and Hyperpigmentation Caused by Exposure to Hazardous Aryl Hydrocarbon Receptor Ligands," Int J Environ Res Public Health, 16(23). https://doi.org/10.3390/ijerph16234864.
[27] Cestari, T. F., Dantas, L. P., and Boza, J. C., 2014, "Acquired Hyperpigmentations," An Bras Dermatol, 89(1), pp. 11-25. https://doi.org/10.1590/abd1806-4841.20142353.
[28] Sarkar, R., Arora, P., Garg, V. K., Sonthalia, S., and Gokhale, N., 2014, "Melasma Update," Indian Dermatol Online J, 5(4), pp. 426-435. https://doi.org/10.4103/2229-5178.142484.
[29] Kang, H. Y., Suzuki, I., Lee, D. J., Ha, J., Reiniche, P., Aubert, J., Deret, S., Zugaj, D., Voegel, J. J., and Ortonne, J.-P., 2011, "Transcriptional Profiling Shows Altered Expression of Wnt Pathway- and Lipid Metabolism-Related Genes as Well as Melanogenesis-Related Genes in Melasma," J Invest Dermatol, 131(8), pp. 1692-1700. https://doi.org/10.1038/jid.2011.109.
[30] Del Bino, S., Duval, C., and Bernerd, F., 2018, "Clinical and Biological Characterization of Skin Pigmentation Diversity and Its Consequences on UV Impact," Int J Mol Sci, 19(9). https://doi.org/10.3390/ijms19092668.
[31] Ortonne, J.-P., Pandya, A. G., Lui, H., and Hexsel, D., 2006, "Treatment of Solar Lentigines," J Am Acad Dermatol, 54(5 Suppl 2), pp. S262-271. https://doi.org/10.1016/j.jaad.2005.12.043.
[32] Goorochurn, R., Viennet, C., Granger, C., Fanian, F., Varin-Blank, N., Roy, C. L., and Humbert, P., 2016, "Biological Processes in Solar Lentigo: Insights Brought by Experimental Models," Exp Dermatol, 25(3), pp. 174-177. https://doi.org/10.1111/exd.12937.
[33] Plensdorf, S., Livieratos, M., and Dada, N., 2017, "Pigmentation Disorders: Diagnosis and Management," Am Fam Physician, 96(12), pp. 797-804.
[34] Morel-Salmi, C., Julia, A., Vigor, C., and Vercauteren, J., 2014, "A Huge PVDF Adsorption Difference Between Resveratrol and ε-Viniferin Allows to Quantitatively Purify Them and to Assess Their Anti-Tyrosinase Property," Chromatographia, 77(13-14), pp. 957-961. https://doi.org/10.1007/s10337-014-2707-8.
[35] "Phytessence White Peony/ Sensuality and Perfect Beauty | Croda Personal Care." [Online]. Available: https://www.crodapersonalcare.com/en-gb/products-and-applications/product-finder/product/2926/Phytessence_1_White_1_Peony.
[36] Kim, S., Lee, J., Jung, E., Huh, S., Park, J.-O., Lee, J., Byun, S. Y., and Park, D., 2008, "Mechanisms of Depigmentation by α-Bisabolol," Journal of Dermatological Science, 52(3), pp. 219-222. https://doi.org/10.1016/j.jdermsci.2008.06.005.
[37] Lee, J., Jun, H., Jung, E., Ha, J., and Park, D., 2010, "Whitening Effect of α-Bisabolol in Asian Women Subjects," International Journal of Cosmetic Science, 32(4), pp. 299-303. https://doi.org/10.1111/j.1468-2494.2010.00560.x.
[38] Eddin, L. B., Jha, N. K., Goyal, S. N., Agrawal, Y. O., Subramanya, S. B., Bastaki, S. M. A., and Ojha, S., 2022, "Health Benefits, Pharmacological Effects, Molecular Mechanisms, and Therapeutic Potential of α-Bisabolol," Nutrients, 14(7), p. 1370. https://doi.org/10.3390/nu14071370.
[39] "Niacinamide PC | IES." [Online]. Available: https://ies-ingredients.com/produit/niacinamide-pc/. [Accessed: 07-Feb-2021].
[40] "AH-CARE G-60 | BASF." [Online]. Available: https://www.carecreations.basf.com/product-formulations/products/products-detail/AH-CARE%20G-60/30530375. [Accessed: 07-Feb-2021].
[41] "X-Pressin C | BASF." [Online]. Available: https://products.basf.com/global/en/em/x-pressin-c.html.
[42] "Phytessence Pink Pomelo EC | CRODA." [Online]. Available: https://www.carecreations.basf.com/product-formulations/products/products-detail/AH-CARE%20G-60/30530375. [Accessed: 07-Feb-2021].
More questions? |
It depends on the type of dark spot (long-term, It depends on the type of dark spot (how established and recent) and skin type. Some will see results after 7 days, others once they have finished a bottle. With twice daily application of the serum for 56 days, 95% of women saw that their dark spots were corrected.*
*Clinical study, % satisfaction, 65 volunteers, 56 days.
The entire collection is suitable for sensitive skin, except the Glycolic Peel Mask, which is not recommended for sensitive skin.
The collection is suitable for use during pregnancy, but only the Vinoperfect Serum has been evaluated by a toxicologist. Its formula contains no substances that could be harmful to the unborn foetus.
Wear sun protection all day long, even in grey weather, and reapply every 2 hours in the event of direct sun exposure.
Yes. Applying the Essence boosts the effectiveness of the Serum which is highly concentrated in dark-spot correcting Viniferine. Applying the Day Cream corrects dark spots and provides radiance immediately. In the evening, the Night Cream promotes cellular renewal for instantly more radiant skin come morning. Finally, adding sun protection to your daily routine minimises the appearance of dark spots.