Zinc gluconate is an agonist of peroxisome proliferator-activated receptor-α in the epidermis.

Abstract

Peroxisome proliferator-activated receptors-α (PPARs-α) are nuclear receptors with anti-inflammatory properties. Zinc gluconate is efficient in the treatment of several inflammatory dermatoses. The aim of our work was to determine whether the modulation of PPAR-α expression and activity could be one of the mechanisms of action of zinc gluconate anti-inflammatory activity in inflammatory dermatoses. Thus, we used ex vivo skin explants incubated with lipopolysaccharide (LPS), a pro-inflammatory molecule, with or without zinc gluconate. We evaluated PPAR-α protein expression using immunohistochemistry, PPAR-α DNA-binding activity using an ELISA-like technique, and PPAR-α mRNA levels using quantitative PCR. On the one hand, we found that PPAR-α epidermal protein expression was stimulated by LPS and that LPS suppressed PPAR-α mRNA expression, without modifying its function. On the other hand, in inflammatory LPS-stimulated explants, zinc gluconate significantly upregulated PPAR-α function and mRNA expression level, without changing its epidermal protein expression. These results suggest that zinc gluconate may be a PPAR-α agonist, which might play a role in the anti-inflammatory activity of this molecule.

• Authors: Carole Poiraud, Gaëlle Quereux, Anne-Chantal Knol, Rémy Allix, Amir Khammari, Brigitte Dreno
• Journal: Experimental dermatology (Exp Dermatol) Vol. 21 Issue 5 Pg. 347-51 (May 2012) ISSN: 1600-0625 [Electronic] Denmark
• PMID: 22509831 (Publication Type: Journal Article)
• Copyright: © 2012 John Wiley & Sons A/S.

Chemical References

• Gluconates
• Lipopolysaccharides
• PPAR alpha
• RNA, Messenger
• gluconic acid

Topics

• Cells, Cultured
• Down-Regulation (drug effects)
• Epidermis (drug effects, metabolism)
• Gluconates (pharmacology)
• Humans
• Lipopolysaccharides (adverse effects, pharmacology)
• PPAR alpha (agonists, genetics, metabolism)
• RNA, Messenger (metabolism)
• Skin Diseases (chemically induced, metabolism)
• Up-Regulation (drug effects)