74 SKIN CARE
120 100 80 60 40 20 0
100 66 57 64 14 Cell (Control) H2 O2
50µg/ml Trolox
H2 O2 +
H2O2 + AHE 1%
H2O2 + AHE 5%
140 120 100 80 60 40 20 0
Figure 6: Effect of 2 % AHE on ROS formation in NHDF cells upon H2O2 treatment (DCFH-DA assay). Values after 3 h exposure to H2O2 were normalised to the value of the control with 100 µM of H2O2.
AHE counteracted the effects of AGEs by influencing the expression of AGE receptors RAGE and AGE-R1 Advanced glycation end products (AGEs) originate from non-enzymatic reactions of proteins with reducing sugars. AGEs also seem to highly accumulate in extrinsically aged skin.8 Previous studies reported that AGEs could
accumulate in dermal elastin and collagens and interact nonspecifically with the cell membrane of dermal fibroblasts.9
Therefore, AGEs may play a role
in skin ageing, since the binding of AGEs with their multiligand receptors, RAGEs, is known to induce oxidative stress and inflammatory responses. However, other AGE-specific cell surface receptors, such as AGE-R1, AGE-R2 and AGE-R3, counteract RAGE function. These receptors are involved in AGE- homeostasis10
, thus reducing AGE levels and
thereby suppressing oxidative stress and inflammation. We therefore investigated the effect of AHE on gene expression patterns of the different classes of AGE receptors. We observed a significant decrease in expression of RAGE genes when cells were incubated with AHE followed by Interleukin 1b (IL-1b) (Fig 8). Furthermore, we also
120 100 80 60 40 20 0
122 100
57 31 14 Controls IL-1ß 10U/ml AHE 1% AHE 2% AHE 2% + IL-1ß
Figure 7: Effect of 2% AHE on RCAN1 expression. GAPDH was used as an internal control for normalisation.
observed a stable up-regulation of AGE-R1 upon incubation with AHE (Fig 9). These results suggest that AHE reduces AGE-induced oxidative stress and inflammatory response by influencing the expression of antagonistic AGE-receptors, RAGE (downregulation) and AGE-R1 (up-regulation).
Induction of wound healing factors In wound re-epithelialization, E-cadherin coordinates tractional forces promoting collective and directional migration of epithelial cells.11 E-cadherin was found to be expressed in two isoforms of different molecular weight: E-cadherin B1 (120kDa) and E-cadherin B2 (90-100kDa). By participating in multiple signalling cascades and the formation of focal adhesions (FA), paxillin plays a critical role during cellular migration and thus, wound healing. 1% AHE induced a 1,6- and 1,3-fold increase of E-cadherin B1 and B2 expression on the injured skin model (Fig 10). Treatment with 5% AHE resulted into 0,8-fold repression of E-cadherin B1 and complete repression of B2 on the injured skin model but 1,5-fold induction of B1 and 1,7-fold induction of B2 on the intact skin model. Paxillin, on the other hand, was 2,4-fold induced when cells were treated with 5% AHE. These results suggest
100 80 67 36 13 Controls
IL-1ß 10 U/ml
AHE 1% AHE 10%
AHE 1% + IL-1ß
AHE 10% + IL-1ß
Figure 8: Effect of 2% AHE extraction on gene expression of advanced glycation end products receptors RAGE in IL-1b stimulated NHDF cells. GAPDH was used as an internal control for normalisation and data were quantified by using the comparative cycle threshold Ct method. Results are expressed as means ± SEM from N=2.
PERSONAL CARE April 2021 82
140 120 100 80 60 40 20 0
that 1% and 5% AHE have a positive effect on wound healing by promoting E-cadherin and paxillin expression in human keratinocytes, respectively.
Advanced pro-ageing A reduction in the levels of functional dermal components such as collagens results in the emergence of clinical ageing features, such as wrinkles and reduced elasticity.12
After 28 days of
treatment with a 2.5% AHE-containing day cream, there was a significant improvement in skin firmness (tensing effect of product) by 4%, viscoelasticity (anti-ageing action of prod.) by 11%, and plasticity by 12% in 43%, 67% and 48% of subjects, respectively. There was also a significant increase in the cutaneous hydration rate by 6% and radiance under the eyes by 17%, consistent with the moisturising and radiant skin effect of the product, respectively (Fig 11a, 11b, 11c).
Enhanced cleansing efficacy 1.5% AHE-enriched facial cleanser exhibited a strong efficacy (about 98%) in eliminating carbon microparticle deposit from skin. There was a significant improvement in the elimination index of the treated group compared to the control group
124 113 100 71 58 36
Controls
IL-1ß 10 U/ml
AHE 1%
AHE 10%
AHE 1% + IL-1ß
AHE 10% + IL-1ß
Figure 9: Effect of 2% AHE extraction on gene expression of advanced glycation end products receptors AGE-R1 in IL-1b stimulated NHDF cells. GAPDH was used as an internal control for normalisation and data were quantified by using the comparative cycle threshold Ct method. Results are expressed as means ± SEM from N=2.
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Normalized fold expression RAGE/GAPDH
% ROS releases (%of Control)
Normalized fold expression AGER1/GAPDH Normalized fold expression RCAN1/GAPDH
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