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Palmitic Acid Induces Production of Proinflammatory Cytokines Interleukin-6, Interleukin-1<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi mathvariant="bold-italic">β</mml:mi></mml:mrow></mml:math>, and Tumor Necrosis Factor-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M2"><mml:mrow><mml:mi mathvariant="bold-italic">α</mml:mi></mml:mrow></mml:math>via a NF-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M3"><mml:mrow><mml:mi mathvariant="bold">κ</mml:mi></mml:mrow></mml:math>B-Dependent Mechanism in HaCaT Keratinocytes — Foodgeist Research
2013peer-reviewed96 citations
Palmitic Acid Induces Production of Proinflammatory Cytokines Interleukin-6, Interleukin-1<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi mathvariant="bold-italic">β</mml:mi></mml:mrow></mml:math>, and Tumor Necrosis Factor-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M2"><mml:mrow><mml:mi mathvariant="bold-italic">α</mml:mi></mml:mrow></mml:math>via a NF-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M3"><mml:mrow><mml:mi mathvariant="bold">κ</mml:mi></mml:mrow></mml:math>B-Dependent Mechanism in HaCaT Keratinocytes
Bingrong Zhou, Mengli Zhang, Qian Zhang, Felicia Permatasari, Yang Xu, Di Wu +2 more
To investigate whether palmitic acid can be responsible for the induction of inflammatory processes, HaCaT keratinocytes were treated with palmitic acid at pathophysiologically relevant concentrations. Secretion levels 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 levels, as well as the cell proliferation ability were measured at the end of the treatment and after 24 hours of recovery. Pyrrolidine dithiocarbamate (PDTC, a selective chemical inhibitor of NF- κ B) and goat anti-human IL-6 polyclonal neutralizing antibody were used to inhibit NF- κ B activation and IL-6 production, respectively. Our results showed that palmitic acid induced an upregulation of IL-6, TNF- α , IL-1 β secretions, accompanied by NF- κ B nuclear translocation and activation. Moreover, the effect of palmitic acid was accompanied by PPAR α activation and Stat3 phosphorylation. Palmitic acid-induced IL-6, TNF- α , IL-1 β productions were attenuated by NF- κ B inhibitor PDTC. Palmitic acid was administered in amounts able to elicit significant hyperproliferation and can be attenuated by IL-6 blockage. These data demonstrate for the first time that palmitic acid can stimulate IL-6, TNF- α , IL-1 β productions in HaCaT keratinocytes and cell proliferation, thereby potentially contributing to acne inflammation and pilosebaceous duct hyperkeratinization.
Extracted Claims
4 claims extracted from this paper into the knowledge graph
compound_effect100% confidence
palmitic acidinducesproduction of proinflammatory cytokines (IL-6, TNF-α, IL-1β)
“Palmitic acid induced an upregulation of IL-6, TNF-α, IL-1β secretions, accompanied by NF-κB nuclear translocation and activation.”
compound_effect100% confidence
palmitic acidinducescell proliferation
“Palmitic acid was administered in amounts able to elicit significant hyperproliferation and can be attenuated by IL-6 blockage.”
compound_effect100% confidence
palmitic acidinducesPPARα activation and Stat3 phosphorylation
“Moreover, the effect of palmitic acid was accompanied by PPARα activation and Stat3 phosphorylation.”
compound_effect100% confidence
palmitic acidinducesNF-κB nuclear translocation and activation
“Palmitic acid induced an upregulation of IL-6, TNF-α, IL-1β secretions, accompanied by NF-κB nuclear translocation and activation.”