Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 55, Issue -, Pages 272-281Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2017.12.024
Keywords
Keratinocytes; Lipopolysaccharide; Protocatechuic acid; Toll-like receptor-4, Akt, mTOR and NF-kappa B pathways; JNK and p38-MAPK
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Protocatechuic acid has demonstrated to have antioxidant and anti-inflammatory effects. We assessed whether protocatechuic acid may reduce the inflammatory mediator production, which is regulated by the Toll-like receptor-4-dependent Akt, mTOR and NF-kappa B pathway, and JNK and p38-MAPK in HaCaT cells and primary keratinocytes. Protocatechuic acid, Akt inhibitor, Bay 11-7085 and N-acetylcysteine reduced the lipopolysaccharide-caused production of cytokines and chemokines, expression of cyclooxygenase, increase in the levels and activities of Toll-like receptor-4, p-Akt and mTOR, activation of NF-kappa B, phosphorylation of the JNK and p38-MAPK, and production of reactive oxygen species in keratinocytes. Inhibitors of the c-JNK (SP600125) and p38-MAPK (SB203580) reduced lipopolysaccharide-caused production of inflammatory mediators, activation of the JNK and p38-MAPK, and production of reactive oxygen species in keratinocytes. These results show that protocatechuic acid may inhibit the lipopolysaccharide-stimulated inflammatory mediator production in keratinocytes by reducing the Toll-like receptor-4-dependent activation of Akt, mTOR and NF-kappa B pathways, and activation of JNK and p38-MAPK. The suppressive effect of protocatechuic acid appears to be associated with inhibition of the reactive oxygen species production. Protocatechuic acid appears to reduce the microbial product-caused inflammatory skin diseases.
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