Conflict of interest: none declared.
Experimental dermatology ● Concise report
Nicotinamide downregulates gene expression of interleukin-6, interleukin-10, monocyte chemoattractant protein-1, and tumour necrosis factor-α gene expression in HaCaT keratinocytes after ultraviolet B irradiation
Article first published online: 12 FEB 2013
© The Author(s) CED © 2013 British Association of Dermatologists
Clinical and Experimental Dermatology
Volume 38, Issue 2, pages 185–188, March 2013
How to Cite
Monfrecola, G., Gaudiello, F., Cirillo, T., Fabbrocini, G., Balato, A. and Lembo, S. (2013), Nicotinamide downregulates gene expression of interleukin-6, interleukin-10, monocyte chemoattractant protein-1, and tumour necrosis factor-α gene expression in HaCaT keratinocytes after ultraviolet B irradiation. Clinical and Experimental Dermatology, 38: 185–188. doi: 10.1111/ced.12018
- Issue published online: 12 FEB 2013
- Article first published online: 12 FEB 2013
- Manuscript Accepted: 7 JUL 2012
Ultraviolet (UV) radiation has profound effects on human skin, causing sunburn, inflammation, cellular-tissue injury, cell death, and skin cancer. Most of these effects are mediated by a number of cytokines produced by keratinocytes. In this study we investigated whether nicotinamide (NCT), the amide form of vitamin B3, might have a protective function in reducing the expression of interleukin (IL)-1β, IL-6, IL-8, IL-10, monocyte chemoattractant protein (MCP)-1 and tumour necrosis factor (TNF)-α in UV-irradiated keratinocytes. HaCaT cells were treated with UVB in the presence or absence of NCT, and cytokine mRNA levels were examined by quantitative real-time PCR. NCT significantly downregulated IL-6, IL-10, MCP-1 and TNF-α mRNA expression, whereas it did not exert any significant effect on IL-1β or IL-8 expression. Because of its ability to decrease these cytokine mediators after UV exposure, NCT is a possible therapy to improve or prevent conditions induced or aggravated by UV light.