Journal Article

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

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

in Carcinogenesis

Volume 27, issue 9, pages 1803-1811
ISSN: 0143-3334
Published online March 2006 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/bgl006
Caffeic acid suppresses UVB radiation-induced expression of interleukin-10 and activation of mitogen-activated protein kinases in mouse

More Like This

Show all results sharing this subject:

  • Clinical Cytogenetics and Molecular Genetics

GO

Show Summary Details

Preview

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 this study, we evaluated the protective effects of CA against UVB radiation-induced IL-10 expression and phosphorylation of MAPKs 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, c-Jun N-terminal protein kinase and p38 mitogen-activated protein kinase, and the downstream transcription factors activator protein-1 and nuclear factor-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.

Journal Article.  6737 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

Full text: subscription required

How to subscribe Recommend to my Librarian

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.