54 SKIN CARE A
120 100 80 60 40 20 0
Control Sebum production (5α-reductase) B
** *
***
120 100 80 60 40 20 0
peptide
µg/mL Zn-
13.5
µg/mL peptide
10
µg/mL Zn
3.5 (corresponding conc.) C
120 100 80 60 40 20 0
Antimicrobial activity against
C.acnes * ** * ** *** * *** ** * *** D Control 3.5/10/13.5 7.0/20/27 28.2/80/108 56.3/160/216
120 100 80 60 40 20 0
Zn/Peptide/Zn-peptide (µg/mL)
µM 10 Retinol Control Keratinization proteins *** ***
*** *** **
****** *
* * * * ***
■ FLG ■ OCLN ■ LCE2C ■ SPRR2E ■ KRT10
for six weeks. Compositions of the tested emulsions
are described in Table 1. The number of inflammatory acne lesions, number of skin pores, overall skin redness and the amount of protoporphyrin IX was determined by an image analysis of whole-face pictures obtained by a VisiaCR camera (Canfield). Sebum was determined by a sebumeter
peptide
µg/mL Zn-
13.5
µg/mL peptide
10
µg/mL Zn
3.5 (corresponding conc.) Pro-inflammatory interleukins
■ IL6 ■ IL8
****** *** ***
Negative control
control UVB peptide
µg/mL Zn-
13.5
µg/mL peptide
10
µg/mL Zn
3.5
(corresponding conc.) UVB
Figure 1: Zn-peptide inhibited all four key events in acne pathogenesis: sebum production (5α-reductase), hyperkeratinization, C. acnes overgrowth and inflammation. When compared to retinol, its effect was similar or even better. Gene expression of (A) 5α-reductase (SRD5A1) and (B) various proteins involved in keratinocyte differentiation: filaggrin (FLG), occludin (OCLN), late cornified envelope 2C protein (LCE2C), small proline rich protein 2E (SPRR2E) and keratin 10 (KRT10) was determined by qRT-PCR in HaCaT keratinocytes treated with Zn-peptide, its individual components (hexapeptide and ZnSO4
*7H2
C. acnes growing in biofilm and treated with the tested compounds for 48 hours. (D) Gene expression of pro-inflammatory interleukins IL-6 and IL-8 was determined by qRT-PCR in HaCaT keratinocytes irradiated with UVB and treated with the tested compounds for 24 hours
A
0 weeks ■ 2 weeks ■ 4 weeks ■ 6 weeks ■ Number of acne lesions
120 100 80 60 40 20 0
Placebo B µM 10 Retinol ****** * µM 10 Retinol
SM815, transepidermal water loss (TEWL) by a tewameter TM300, elasticity by a cutometer dual MPA580 (all Courage-Khazaka electronics), wrinkle depth by a Primos 3D camera (Canfield), and collagen level by reflectance confocal microscopy (Vivascope 3000, Mavig).
Statistical analysis T test was used for the statistical evaluation of the results. *p< 0.05, **p<0.01, ***p<0.001 in comparison to the respective controls or placebo if not stated otherwise.
Results and discussion Inhibition of sebum production (5α-reductase) An increased production of sebum is considered one of the key events in the pathogenesis of acne. Among the most potent stimulators of sebum production are androgens whose upregulation is often associated with acne development.2 Within the skin cells, testosterone, the
most common androgen, is quickly reduced to 5α-dihydrotestosterone (DHT) by enzyme 5α-reductase.3
Both testosterone and DHT
bind to androgen receptors (ARs) promoting sebum production. However, DHT is five to ten times more potent AR activator.4
In O) of corresponding concentrations and retinol for 72 hours. (C) Antimicrobial activity towards
the skin of acne patients, 5α-reductase is commonly upregulated leading to the higher rate of conversion of testosterone to DHT and increased sebum production.5 Zn-peptide complex significantly inhibited
gene expression of 5α-reductase. It was more effective than its individual components of
Zn peptide 13.5 µg/mL
* * *** 0 weeks 6 weeks 0 weeks 6 weeks Retinol 0.2% 0 weeks 6 weeks
Zn-peptide 13.5 µg/mL
Retinol 0.2%
0 weeks
6 weeks
0 weeks
6 weeks
0 weeks
6 weeks
Figure 2: Zn-peptide decreased the number of acne lesions and improved the overall appearance of acne-prone skin better than retinol. The number of acne lesions was determined by an image analysis of the whole-face images: (A) quantification, (B) representative images
PERSONAL CARE July 2023
www.personalcaremagazine.com
0D590 (% of control) Number of acne (% of placebo)
Relative gene expression (% of respective control)
Relative gene expression (% of respective UVB control)
Relative gene expression (% of respective control)
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