Inhibiting Cathepsin G to Protect Against Photoaging and Infra’aging

Sep 1, 2013 | Contact Author | By: Estelle Loing, PhD; Elisabeth Lamarque; Carine Bezivin; and Magali Borel, Lucas Meyer Cosmetics
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Title: Inhibiting Cathepsin G to Protect Against Photoaging and Infra’aging
photoagingx infra’agingx wrinklesx cathepsin Gx MMP-1x
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Keywords: photoaging | infra’aging | wrinkles | cathepsin G | MMP-1

Abstract: Ultraviolet and infrared exposure are sources of premature skin aging, characterized by solar elastosis and extracellular matrix degradation. Polygonum aviculare extract is a cathepsin G inhibitor, and is shown here to oppose photoaging and infra’aging by improving skin firmness and elasticity, in turn reducing the appearance of wrinkles.

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E Loing, E Lamarque, C Bezivin and M Borel, Inhibiting Cathepsin G to Protect Against Photoaging and Infra’aging, Cosm & Toil 128(9) 658 (2013)

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Photoaging refers to premature skin aging that results from chronic exposure to solar radiation or other sources that mimick solar effects. Until recently, photoaging essentially was linked to the ultraviolet (UV) portion of the solar spectrum; specifically, to UVB and UVA rays with wavelengths in the 290–400 nm range. UVB is absorbed by chromophores in the epidermis and is responsible for sunburn, whereas the less energetic UVA penetrates more deeply into the dermis and is associated with premature aging. Both UVB and UVA may also cause cancer and immunosuppression.1, 2

However, the solar spectrum is much broader, and attention is now turning toward infrared radiation (IR), i.e., the 760 nm–1 mm end of the rainbow. IR can be divided into IRA, IRB and IRC, and while all three have low energy and may seem inoffensive, IRA penetrates deeply into the skin, even reaching the hypodermis (see Figure 1).3, 4 Moreover, nearly half of solar rays fall into the IR range, of which 30% is IRA, versus around just 5% for UV.3 As a consequence, any effect of IRA on skin physiology deserves a closer look.

The hallmark of photoaged skin is an accumulation of elastolytic material in the upper and middle dermis, which occurs through a process known as solar elastosis.5 Together with collagen, elastic fibers normally form a support for cell attachment, since dermal fibroblasts need such anchoring to function properly. Chronic sun exposure activates various proteases that dismantle the extracellular matrix (ECM) scaffold, leaving amorphous material behind.

Cathepsin G has recently emerged as an important mediator of proteolytic ECM degradation in photoaging. This serine protease is secreted by inflammatory neutrophils and dermal fibroblasts. It is present in higher amounts in aged human skin than in younger skin, and its expression and/or activity can be further increased with UVA exposure.6, 7 Further, in one animal model of photoaging, a cathepsin G inhibitor prevented UVB-induced ECM degradation, suggesting activation of the enzyme by UVB as well.8

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Figure 1. IR can be divided into IRA, IRB and IRC; IRA in particular penetrates deeply into the skin, even reaching the hypodermis.

Figure 1. IR can be divided into IRA, IRB and IRC; IRA in particular penetrates deeply into the skin, even reaching the hypodermis.

IR can be divided into IRA, IRB and IRC, and while all three have low energy and may seem inoffensive, IRA penetrates deeply into the skin, even reaching the hypodermis (see Figure 1).3, 4

Figure 2. Neat inhibition of cathepsin G activity with increasing concentrations of the extract

Figure 2. Neat inhibition of cathepsin G activity with increasing concentrations of the extract

Results presented in Figure 2 show a neat inhibition of cathepsin G activity with increasing concentrations of the extract, with an IC50 value of 0.014%.

Figure 3. Results from MMP-1 immunolabeling; pre-treatment with the extract prevented a UV-induced increase in MMP-1 expression.

Figure 3. Results from MMP-1 immunolabeling; pre-treatment with the extract prevented a UV-induced increase in MMP-1 expression.

Results from MMP-1 immunolabeling are presented in Figure 3.

Figure 4. Immunostaining of fibrillin-1

Figure 4. Immunostaining of fibrillin-1

As can be seen in Figure 4, immunostaining of fibrillin-1 revealed a strong expression of the protein in control samples, with regular distribution at the dermal-epidermal junction (DEJ) and in the upper dermis.

Figure 5. Results from MMP-1 immunolabeling; pre-treatment with the extract prevented an IR-induced increase in MMP-1 expression.

Figure 5. Results from MMP-1 immunolabeling; pre-treatment with the extract prevented an IR-induced increase in MMP-1 expression.

Results from MMP-1 immunolabeling are presented in Figure 5.

Figure 6. Immunostaining of tropoelastin on day nine frozen skin sections; reduced tropoelastin expression was alleviated when pre-treating with Polygonum aviculare extract.

Figure 6. Immunostaining of tropoelastin on day nine frozen skin sections; reduced tropoelastin expression was alleviated when pre-treating with <em>Polygonum aviculare</em> extract.

The same technique was used for immunostaining of tropoelastin on day nine frozen skin sections.

Figure 7. Results from viscoelastic measurements: a) firmness and b) elasticity (D28)

Figure 7. Results from viscoelastic measurements: a) firmness and b) elasticity (D28)

Results from viscoelastic measurements are shown in Figure 7.

Figure 8. Results from skin topography measurements in the crow’s feet area

Figure 8. Results from skin topography measurements in the crow’s feet area

Results from skin topography measurements in the crow’s feet area are shown in Figure 8.

Figure 9. A selection of photographs representative of the clinical results described

Figure 9. A selection of photographs representative of the clinical results described

A selection of photographs, representative of the clinical results described, are presented in Figure 9.

Figure 10. Protective effects are seen at all skin levels, opposing UVB at the epidermis as well as UVA and IRA at the dermis.

Figure 10. Protective effects are seen at all skin levels, opposing UVB at the epidermis as well as UVA and IRA at the dermis.

Its protective effects are seen at all skin levels, opposing UVB at the epidermis as well as UVA and IRA at the dermis (see Figure 10).

Footnotes (CT1309 Loing)

a Elix-IR (INCI: Polygonum Aviculare extract) is a product of Lucas Meyer Cosmetics, www.lucasmeyercosmetics.com.
b The Lourmat RMX 3W UV simulator is manufactured by Vilber, www.vilber.com.
c The IR lamp described is manufactured by Dr. Fisher, www.dr-fischer-group.com.
d The MPA 580 Cutometer is a device from Courage-Khazaka GmbH, www.courage-khazaka.com.
e The Visio3D DermaTOP BLUE system is a device from Eotech SA, www.eotech-sa.com.

Formula 1. Test formulation used in the clinical study

Formula 1. Test formulation used in the clinical study

All subjects were asked to blindly apply a test and control cream (see Formula 1) containing, or not, 2% Polygonum aviculare extract.

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