Premium
Zinc gluconate is an agonist of peroxisome proliferator‐activated receptor‐α in the epidermis
Author(s) -
Poiraud Carole,
Quereux Gaëlle,
Knol AnneChantal,
Allix Rémy,
Khammari Amir,
Dreno Brigitte
Publication year - 2012
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2012.01467.x
Subject(s) - peroxisome proliferator activated receptor , receptor , lipopolysaccharide , downregulation and upregulation , chemistry , peroxisome , agonist , peroxisome proliferator activated receptor delta , endocrinology , zinc , ppar agonist , inflammation , nuclear receptor , medicine , biology , biochemistry , transcription factor , organic chemistry , gene
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.