Effects of different kinds of pollutants on the lipidic metabolism of human sebocytes and protective effects of a new macroalgae culture extract
Catherine KERN1, Erwan LE GÉLÉBART2, Laetitia CATTUZZATO, Sevda CORDIER-DIRIKOC3, Nathalie PEDRETTI3, François-Xavier BERNARD3, Sandy DUMONT1, Carla PEREZ4
1SEPPIC – Innovation Direction – 127 chemin de la Poudrerie BP90228, 81105 Castres cedex, France
2BiotechMarine – Innovation Direction – ZI BP72, 22260 Pontrieux, France
3Bioalternatives SAS – 1bis rue des plantes – BP N°50011, 86 160 Gençay, France
4SEPPIC – 819 West Nanjing Rd, Room 1508 Zhongchuang Building, Shangai 200041, China
Introduction
Pollution is a global health concern. Skin, being the interface between body and environment, is challenged everyday by atmospheric pollutants (particulate matters , toxic gases, indoor pollutants,…) which contribute to skin disorders such as psoriasis, atopic dermatitis, skin cancer, skin ageing, pigmentary disorders and acne [1–4].
Pollutants are supposed to act through 4 biological mechanisms:
- generation of free radicals
- induction of inflammatory cascades
- activation of aryl hydrocarbon receptor (AhR)
- alteration of cutaneous microflora [5, 6].
Our previous investigations showed that:
- Both sebocytes lipid production and skin sebum production are stimulated by some pollutants.
- Ame* acts as a urban life dermopurifying ingredient, by protecting epidermal cells from cadmium, human sebocytes from urban dust and skin from ozone.
Materials & Methods
Results & Discussion
1) Lipid droplet formation
Pollution: Increase lipid formation.
Ame: Decrease lipid formation (with urban dust)
2) Neutral lipidic neosynthesis
Conversion of fatty acids into triglycerides:
Increase with pollution
Decrease with Ame
3) Transcriptomic regulations (24h)
Only a few regulations observed with pollutants or Ame.
Putative regulated mechanisms:
Cyp-pathways
antioxydant defenses
Conclusion
Our results:
Enlighten new pollution-induced metabolic regulation of the lipid profile of stimulated sebocytes.
Suggest that underlying mechanisms are more likely to occur at the metabolic level than at the transcriptional level.
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