SKIN CARE -AHE +AHE 1.0%
0.7 0.6 0.5 0.4 0.3 0.2 0.1 0
0
Figure 2: Maintaining Biodiversity of the Microbiome with and without 1% AHE.
the expression pattern of CK10 and CK16 in HaCaT cells with and without AHE-treatment, respectively. Western blot analysis revealed an induction of CK10 in extracts obtained from HaCaT cells after treatment with AHE. Furthermore, this effect was reinforced when the cells were pre-stimulated with C. acnes.
Repression of pro-inflammatory cytokines A continuous expression of cytokines following noxious stress causes chronic inflammation and skin damage which in turn leads to skin disease and (premature) ageing.3
Our in vitro
irritation study demonstrated the anti- inflammatory activity of AHE by suppressing the induction of inflammatory markers, such as tumour necrosis factor α (TNF-α), interleukin-1b (IL-1b), interleukin-6 (IL-6), and interleukin-8 (IL-8) in peripheral blood mononuclear cells (PBMCs) and reconstructed human epidermis (RHE) after stimulation with C. acnes. These results suggest a role for AHE in the prevention of inflammatory skin diseases and premature ageing by suppressing pro- inflammatory cytokines (Fig 4).
600 500 400 300 200 100 0
5 10 15 20 Time [h] Figure 3: Growth Curve of S. epidermidis with and without 1% AHE.
AHE inhibits the production of NO, 8-Isoprostanes and PGE2 Age-related functional losses and diseases are associated with accumulation of reactive oxygen (ROS) and nitrogen species,4
such as
nitrogen monoxide (NO). Most Isoprostanes are produced by ROS that catalyse lipid peroxidation. Measurement of Isoprostanes is an accurate way to assess oxidative stress in vivo and can be correlated with numerous diseases.5 Prostaglandin E2 (PGE2)-induced inhibition of collagen expression and promotion of Matrix- Metalloprotease-1 (MMP1), respectively, are two further mechanisms related to ageing.6
In
this study we investigated the effect of AHE on lipopolysaccaride (LPS)-induced formation of NO, 8-Isoprostane and PGE2 in RAW cells (Fig 05). Treatment with AHE elicited a marked decrease in the formation of NO and 8-Isoprostane as compared to the LPS-treated controls. Additionally, the expression of PGE2 was
reduced by half upon treatment with 2% AHE. These data indicate that AHE exerts an anti-ageing effect due to the reduction of oxidative stress markers, such as NO and 8-Isoprostane, and PGE2.
CON ■ STIM ■ CC 1% ■ BIS 1% ■ TNF α IL 1b IL-6 IL-8
Figure 4: AHE-induced repression of inflammatory cytokines TNF-a, IL-1b, 1L-6, and IL- 8 after stimulation of reconstructed human epidermis (RHE) with C. acnes. (control – nonstimulated, untreated RHE; STIM – stimulation with C. acnes, no treatment; AHE 1% - stimulation followed by treatment with 1% Alpin Heilmoor Extract, CC – stimulation followed by treatment with 1% charcoal; BIS – stimulation followed by treatment with 1% Bisabolol).
www.personalcaremagazine.com
120 100 80 60 40 20 0
AHE inhibits the formation of ROS and suppresses the expression of RCAN1 The reduction of oxidative stress by reactive oxygen species (ROS) scavengers followed by the delay of the age-associated decline in physiological processes and marked prolongation in the mean lifespan can be considered as a confirmation of the oxidative stress theory of ageing. Mitochondria are primary sites for ROS
accumulation. Regulator of calcineurin-1 (RCAN1) regulates mitochondrial functions and increases the susceptibility to oxidative stress.7
Here we
determined whether AHE produces a reduction in ROS as a marker of oxidative stress by using NHDF cells and H2
O2 as a model of oxidative stress. We also
investigated the effect of AHE on RCAN1 expression. Our data showed that AHE-treatment has a
significantly reductive effect on the formation of ROS compared to Trolox (Trolox is an antioxidant and a structural analogue of vitamin E) positive controls (Fig 6). Furthermore, a significant decrease in expression of RCAN1 could be observed (Fig 7). These data indicate that AHE is a potent inhibitor
of ROS formation and can be used as an anti-ageing agent through the oxidative stress pathway.
LPS (Control) ■ LPS + 1% AHE ■ LPS + 2% AHE ■ 100 76.8 59.5 44.6 23.3 N0 8-Isoprostane PGE2
Figure 5: Effect of 1% and 2% AHE on nitrogen monoxide (NO), 8-Isoprostane and Prostaglandin E2 (PGE2) formation in RAW cells. Data were normalized as percentage of negative control with LPS (100ng/ml). Results are expressed as means ± SEM from N=2.
April 2021 PERSONAL CARE 100 91.7 100 87 25 30 35 40 - AHE ■ +1% AHE ■
73
Inhibitions rate (% of Control)
100 117
138 65 100 335 117 160 65 100 161
489 500
464 100 125
233 238
353 Optical Densit 576nm
335
% of Control
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