Palmitic acid induces production of proinflammatory cytokines interleukin-6, interleukin-1β, and tumor necrosis factor-α via a NF-κB-dependent mechanism in HaCaT keratinocytes.

Palmitic acid induces production of proinflammatory cytokines interleukin-6, interleukin-1β, and tumor necrosis factor-α via a NF-κB-dependent mechanism in HaCaT keratinocytes.

To research whether or not palmitic acid will be answerable for the induction of inflammatory processes, HaCaT keratinocytes have been handled with palmitic acid at pathophysiologically related concentrations. Secretion ranges of interleukin-6 (IL-6), tumor necrosis factor- α (TNF- α), interleukin-1 β (IL-1 β), NF- κ B nuclear translocation, NF- κ B activation, Stat3 phosphorylation, and peroxisome proliferator-activated receptor alpha (PPAR α) mRNA and protein ranges, in addition to the cell proliferation capacity have been measured on the finish of the therapy and after 24 hours of restoration.
Pyrrolidine dithiocarbamate (PDTC, a selective chemical inhibitor of NF- κ B) and goat anti-human IL-6 polyclonal neutralizing antibody have been used to inhibit NF- κ B activation and IL-6 manufacturing, respectively. Our outcomes confirmed that palmitic acid induced an upregulation of IL-6, TNF- α , IL-1 β secretions, accompanied by NF- κ B nuclear translocation and activation. Furthermore, the impact of palmitic acid was accompanied by PPAR α activation and Stat3 phosphorylation.
Palmitic acid-induced IL-6, TNF- α , IL-1 β productions have been attenuated by NF- κ B inhibitor PDTC. Palmitic acid was administered in quantities in a position to elicit vital hyperproliferation and will be attenuated by IL-6 blockage. These knowledge reveal for the primary time that palmitic acid can stimulate IL-6, TNF- α , IL-1 β productions in HaCaT keratinocytes and cell proliferation, thereby probably contributing to pimples irritation and pilosebaceous duct hyperkeratinization.

Leave a Reply

Your email address will not be published.