EFFICIENCY Advanced glycation end products DISCOVER OUR COMPLETE - - PowerPoint PPT Presentation

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EFFICIENCY Advanced glycation end products DISCOVER OUR COMPLETE - - PowerPoint PPT Presentation

ANTI - AGEING EFFICIENCY Advanced glycation end products DISCOVER OUR COMPLETE IN-VITRO A main consequence of oxidatjve stress is the EVALUATION METHODS appearance of protein glycatjon and advanced glycatjon end products (AGEs) during life


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SLIDE 1

Advanced glycation end products Extracellular matrix components Detoxification Age spots Oxidative stress

LC3-II

CEL CML

JNK

HMOX ERK1/2

p38 Nrf2

Jak/STAT Structural and functjonal components of the ECM are profoundly disrupted during skin ageing processes resultjng in weakened contractjon of collagen fjbers, decrease of elas- tjn and proteoglycans abundance, increased metalloproteases actjvity, etc. Ageing process leads to pigmentatjon disorders (skin macular lesions) of variable melanin content which generally increase (senile lentjgo). Rencent data also suggest a link between environmental pollutjon, ageing signs, and increased age spots. A main consequence of oxidatjve stress is the appearance of protein glycatjon and advanced glycatjon end products (AGEs) during life tjme, damaging skin cell membranes. AGEs are directly involved in damage and loss of ECM components, the appearance of roughness, uneven tone, brown patches, thin skin and deep wrinkles.

ANTI - AGEING

EFFICIENCY

DISCOVER OUR COMPLETE IN-VITRO

EVALUATION METHODS

Healthy skin relies on many endogenous sys- tems to insure repair, disposal or recycling of disrupted biological components. These include machineries of the proteasome, lysosome, auto- phagy, DNA damage and repair, NRF2 pathway, unfolded protein response, etc. Exhaustjon of the endogenous antjoxidatjve machinery is incriminated in skin ageing. Overall oxidatjve stress can be measured in presence or absence of external factors, as well as mitochondrial complex II abun- dance which is inversely correlated with skin ageing.

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SLIDE 2

enzymatic conversion

Tyrosinase and tyrosinase-related proteins (TRP-1/2) are the critjcal me- lanogenic enzymes responsible for me- lanin synthesis.

melanogenic pathways

The complex & dynamic process of melanogenesis involves an extensive intercellular cross-talk that actjvates signalling responses such as MC1-R pathway actjvatjon.

melanosome transfer

Melanosomes are transferred to sur- rounding keratjnocytes in which they localize to the perinuclear area.

melanosome maturation

During their maturatjon, melanosomes move towards the extremity of dendrites through a microtubule-dependant intracellular transport.

transcriptional regulation

MITF is a major transcriptjon factor that regulates melanocyte functjon from their development to their response to environmental stjmuli con- trolling melanosome formatjon and expression

  • f melanogenic enzymes.

CHALLENGING

SKIN PIGMENTATION

DISCOVER OUR ExCLusivE in vitro DEVICE

DERMOSCOPY

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SLIDE 3

LOR IVL FLG TEER IL6 IL8 TNFα IL1 PGE2 LTB4 NF-кB

UBD 60µM UBD 20µM CTRL

BARRIER DISRUPTION

  • 28%-40%

Defects in the protectjve physical barrier lead to a decrease in expression of difgerentjatjon markers such as fjlaggrin (FLG), involucrin (IVL), loricrin (LOR) & trans-epithelial electrical resistance (TEER) while facilitatjng allergens/pathogens invasion.

NF-кB TRANSLOCATION

Increased nuclear translocatjon of NF-кB is an important pathogenic factor involved in many acute & chronic infmammatory disorders.

+18%

CYTOKINES & CHEMOKINES RELEASE

Productjon of primary proinfmammatory cytokines prostaglandin E2 (PGE2), leukotriene B4 (LTB4), in- terleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), & tumour necrosis factor-ɑ (TNF-ɑ).

P M A REF . CTRL PREVENTIVE P M A REF . CTRL CURATIVE

x10

  • 61%

x19

  • 64%

MORPHOLOGICAL CHANGES

Infmammatory dermatoses are characterized by the presence of abnormal keratjnocyte proliferatjon (acanthosis) or accumulatjon of intraepidermal edema (spongiosis) observed in psoriasis & AD, respectjvely.

RHE RHE-PSO +29% PMA UbD UV s

acute inflammation chronic inflammation

Sensitive Skin

INFLAMMATION ATOPIC DERMATITIS PSORIASIS

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SLIDE 4

Discover our

TRANSCRIPTOMICS TOOLS

for TARGET IDENTIFICATION

& mechanism of action

LIPID SYTNHESIS & TRANSPORT ANTIMICROBIAL DEFENSE DIFFERENTIATION & EPIDERMAL BARRIER CELL JUNCTIONS LIPID HOMEOSTASIS BARRER RECOVERY INFLAMMATION & CHEMOTAXIS PRURITUS

Epidermal Benefits

EXTRA CELLULAR MATRIX MODELING AUTOPHAGY & RECYCLING CELLULAR SENESCENCE OXYDATIVE STRESS RESPONSE

dermal Benefits Skin BARRIER & Tissue Cohesion

AGE SPOTS MELANOGENESIS DEPIGMENTATION

Pigmentation Pollution & DEtoxification

HMOX Nrf2 RECYCLING & DETOXIFICATION DRUG METABOLISM DNA DAMAGE REPAIR cyp450 AGE SPOTS h h h Oh h
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SLIDE 5

DNA damage & repair

If not controlled, DNA alteratjons could afgect cell cycle and induce apoptosis. Autophagy has a pivotal role in recycling damaged non-functjonal

  • rganelles &

unfolded proteins.

inflammatory response drug metabolism

The cytoplasmic xeno-sensor AhR leads to inductjon of xenobiotic-responsive elements such as CYP proteins family.

  • xidative stress

response

The depletjon in enzy- matjc and nonenzymatjc antjoxidant capacity leads to a chronic and vicious

  • xidatjve state.

unfolded protein response

Among others, Matrix MetalloProteinases contribute to matrix modulatjon that af- fects cell-cell/matrix interactjons critjcal for skin integrity.

Matrix modelling

keratjnocyte

  • r fjbroblast

Pollutants stjmulate the re- lease of pro-infmammatory mediators such as PGE2 & IL cytokines.

POLLUTION

AND ENVIRONMENTAL STRESSES