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Mediators of Inflammation
Volume 2013, Article ID 530429, 11 pages
http://dx.doi.org/10.1155/2013/530429
Research Article

Palmitic Acid Induces Production of Proinflammatory Cytokines Interleukin-6, Interleukin-1 , and Tumor Necrosis Factor- via a NF- B-Dependent Mechanism in HaCaT Keratinocytes

Department of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China

Received 9 May 2013; Revised 23 July 2013; Accepted 24 July 2013

Academic Editor: Salahuddin Ahmed

Copyright © 2013 Bing-rong Zhou et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Supplementary Material

Supplementary Figure: Effect of NF-κB inhibitor PDTC on HaCaT cell viability and PA–induced NF-κB activation. (A) HaCaT cells were untreated or exposed to PDTC (10, 50, 100 μmol/L) for 1 hour. Cell viability was measured by a CCK-8 assay kit. Data are expressed as mean ± standard deviation (n = 5). ∗P < 0.05 compared with control. (B) HaCaT cells were untreated or exposed to 0.15 mM palmitic acid (PA) for 24 hours, either without or with pretreatment for 1 hour with 10 μmol/L PDTC or 0.1% dimethylsulfoxide (DMSO, as vehicle control). IKKα and IκBα expression levels were measured by western blotting. Each experiment was done in triplicate. Data are mean ± standard deviation. ∗P < 0.05 compared with PA.

  1. Supplementary Figure