Journal
PHARMACOLOGICAL RESEARCH
Volume 59, Issue 5, Pages 330-337Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.phrs.2009.01.009
Keywords
Resveratrol; Pro-inflammatory cytokine; COX-2; Intracellular Ca2+; NF-kappa B; MAPKs
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Funding
- Ministry of Commerce, Industry and Energy (MOCIE) in the Republic of Korea [RTI 05-03-02]
- National Research Foundation of Korea [핵C6A3403] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Resveratrol is a phytoalexin polyphenolic compound found in various plants, including grapes,berries, and peanuts. Recently, studies have documented various health benefits of resveratrol including cardiovascular and cancer-chemopreventive properties. The aim of the present study was to demonstrate the effects of resveratrol on the expression of pro-inflammatory cytokines, as well as to elucidate its mechanism of action in the human mast cell line (HMC-1). Cells were stimulated with phorbol 12-myristate 13-acetate (PMA) plus A23187 in the presence or absence of resveratrol. To study the possible effects of resveratrol, ELISA, RT-PCR, real-time RT-PCR, Western blot analysis, fluorescence, and luciferase activity assays were used in this study. Resveratrol significantly inhibited the PMA plus A23187-induction of inflammatory cytokines such as tumour necrosis factor (TNF)-alpha, interleukin (IL)-6 and IL-8. Moreover, resveratrol attenuated cyclooxygenase (COX)-2 expression and intracellular Ca2+ levels. In activated HMC-1 cells, phosphorylation of extra-signal response kinase (ERK) 1/2 decreased after treatment with resveratrol. Resveratrol inhibited PMA plus A23187-induced nuclear factor (NF)-kappa B activation, I kappa B degradation, and luciferase activity. Resveratrol suppressed the expression of TNF-alpha, IL-6, IL-8 and COX-2 through a decrease in the intracellular levels of Ca2+ and ERK 1/2, as well as activation of NF-kappa B. These results indicated that resveratrol exerted a regulatory effect on inflammatory reactions mediated by mast cells. (C) 2009 Published by Elsevier Ltd.
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