Kang Ok-Hwa, Jang Hye-Jin, Chae Hee-Sung, Oh You-Chang, Choi Jang-Gi, Lee Young-Seob, Kim Jong-Hak, Kim Youn Chul, Sohn Dong Hwan, Park Hyun, Kwon Dong-Yeul
College of Pharmacy and Wonkwang-Oriental Medicines Research Institute, Wonkwang University, Iksan, Jeonbuk 570-749, Republic of Korea.
Pharmacol Res. 2009 May;59(5):330-7. doi: 10.1016/j.phrs.2009.01.009. Epub 2009 Jan 29.
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)-kappaB activation, IkappaB 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-kappaB. These results indicated that resveratrol exerted a regulatory effect on inflammatory reactions mediated by mast cells.
白藜芦醇是一种植物抗毒素多酚类化合物，存在于多种植物中，包括葡萄、浆果和花生。最近，研究记录了白藜芦醇的各种健康益处，包括心血管保护和癌症化学预防特性。本研究的目的是证明白藜芦醇对促炎细胞因子表达的影响，并阐明其在人肥大细胞系（HMC-1）中的作用机制。在有或没有白藜芦醇的情况下，用佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）加A23187刺激细胞。为了研究白藜芦醇的可能作用，本研究使用了酶联免疫吸附测定（ELISA）、逆转录聚合酶链反应（RT-PCR）、实时RT-PCR、蛋白质免疫印迹分析、荧光和荧光素酶活性测定。白藜芦醇显著抑制PMA加A23187诱导的炎性细胞因子，如肿瘤坏死因子（TNF）-α、白细胞介素（IL）-6和IL-8。此外，白藜芦醇减弱了环氧合酶（COX）-2的表达和细胞内钙离子水平。在用白藜芦醇处理后，活化的HMC-1细胞中细胞外信号调节激酶（ERK）1/2的磷酸化减少。白藜芦醇抑制PMA加A23187诱导的核因子（NF）-κB活化、IκB降解和荧光素酶活性。白藜芦醇通过降低细胞内钙离子和ERK 1/2水平以及激活NF-κB来抑制TNF-α、IL-6、IL-8和COX-2的表达。这些结果表明，白藜芦醇对肥大细胞介导的炎症反应具有调节作用。
