Volume XXVII - Nr.1 - November 2012
Filagrinol
NEW ACQUISITIONS ON THE MECHANISM OF ACTION OF FILAGRINOL
Filagrinol
® is an active composed by
unsaponifiable fractions of olive, soybean, wheat germ oil and pollen extract. The studies carried out in the 80’s demonstrated that
Filagrinol stimulates filaggrin production,
an essential protein that promotes organization and aggregation of keratin and enhances the NMF (Natural Moisturizing Factor), a pool of low-weight
hydrophilic molecules which bind water, necessary for both skin hydration and integrity.
Therefore Filagrinol
is an active epidermal moisturizer that assures integrity of skin, fundamental to guarantee its physiological barrier function.
Based on the latest scientific discoveries, the mechanism by which a lipid-based substance such as
Filagrinol
can affect the protein synthesis of pro-filaggrin is now clearer. Therefore a hypothesis on the mechanism of action of
Filagrinol
at the level of the nucleus of the keratinocyte will follow. The substances of lipid nature constituting
Filagrinol act as primary messenger, in fact,
to work they must interact with specific receptors which then act in the nucleus of epithelial cell and stimulate in the direction of protein synthesis of pro-filaggrin.
Furthermore Filagrinol
easily goes directly to the nucleus where there are nuclear receptors for lipids passing the phospholipid bilayer of the membrane.
These receptors, activated by their specific ligand, directly activate or deactivate specific genes of the target cell.
Moreover recent scientific discoveries have identified 48 genes coding for many nuclear lipid receptors.
These include, besides the classical hormone receptors for steroids and liposoluble vitamins, a large group that has been called "nuclear lipid receptors orphans"
whose functions are not yet fully known (1). Among them there is the PPAR “Peroxisome proliferator-activated receptor”, which stimulates the keratinic differentiation,
decreases proliferation of keratinocytes, accelerates the shelter of the impermeable barrier and increases epidermal lipid synthesis and finally reduces skin inflammation.
This receptor is activated by fatty acids, prostaglandins, eicosanoids and other lipid metabolites. Experiments on keratinocytes in culture have shown that stimulation
of the PPAR receptor produces an increase of proteins related to the differentiation, including profilaggrin (2).
Therefore today is safe to postulate the hypothesis that Filagrinol
with its pool of lipid substances goes right to bind the nuclear receptor PPAR activating lipid synthesis of filaggrin.
Bibliography
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Chawla A, Repa JJ, Evans RM, Mangelsdorf DJ. Nuclear receptors and lipid physiology: opening the X-files. Science. 2001 Nov 30;294(5548):1866-70.
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Man MQ, Barish GD, Schmuth M, Crumrine D, Barak Y, Chang S, Jiang Y, Evans RM, Elias PM, Feingold KR. Deficiency of PPARbeta/delta in the epidermis results in defective cutaneous permeability barrier homeostasis and increased inflammation. J Invest Dermatol. 2008 Feb;128(2):370-7. Epub 2007 Aug 23.