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Carcinogenesis Advance Access published online on March 8, 2006
Carcinogenesis, doi:10.1093/carcin/bgl006
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received October 13, 2005
Revised February 20, 2006
Accepted March 3, 2006

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Caffeic acid suppresses UVB radiation-induced expression of interleukin-10 and activation of mitogen-activated protein kinases mouse

Vanisree Staniforth 1, Lu-Tang Chiu 1, and Ning-Sun Yang 1 *

1 Institute of BioAgricultural Sciences, Academia Sinica, Taipei 115, Taiwan, ROC

* To whom correspondence should be addressed.
Ning-Sun Yang, E-mail: nsyang{at}gate.sinica.edu.tw


  Abstract

Ultraviolet B (UVB) radiation present in sunlight causes sustained immune suppression, photocarcinogenesis and photoaging in humans. Interleukin-10 (IL-10) plays a critical role in UVB-induced immune suppression by inhibiting cell-mediated immune reactions. Mitogen-activated protein kinases (MAPKs) have been implicated in UVB-induced skin carcinogenesis. Caffeic acid (CA), a phenolic acid present in many dietary plants has been shown to confer antioxidant, anti-inflammatory and anticancer activities. In the present study, we evaluated the protective effects of CA against UVB radiation-induced IL-10 expression and phosphorylation of mitogen-activated protein kinases in mouse skin. An in vivo transgenic IL-10 promoter-luciferase reporter gene based assay revealed that CA inhibits the transcriptional activation of UVB-induced IL-10 promoter. This was further confirmed by significant inhibition of UVB radiation-induced IL-10 mRNA expression and protein production by CA in mouse skin. Contact hypersensitivity assay showed that CA could attenuate the local immune suppression induced by UVB radiation against a hapten, dinitrofluorobenzene. Our results indicated that CA might inhibit IL-10 production by interfering with an early step, prostaglandin E2 synthesis, in the activation of UVB-induced immune suppressive cytokine cascade. CA also significantly inhibited the UVB-induced activation of MAPK signal transduction pathways, such as extracellular signal-regulated protein kinase (ERK), c-Jun N-terminal protein kinase (JNK) and p38 mitogen-activated protein kinase (p38), and the downstream transcription factors activator protein-1 (AP-1) and nuclear factor kappa B (NF-{kappa}B). The findings of our study suggest that CA may confer significant protection against UVB-induced immune suppression and photocarcinogenesis in vivo and provide the possible underlying molecular basis for its actions. Therefore, CA may have therapeutic potential as a topical protective agent against the deleterious effects of UVB radiation.


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