Soy isoflavones (daidzein & genistein) inhibit 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced cutaneous inflammation via modulation of COX-2 and NF-κB in Swiss albino mice
Soy isoflavones (daidzein & genistein) inhibit 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced cutaneous inflammation via modulation of COX-2 and NF-κB in Swiss albino mice
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DOI：
10.1016/j.tox.2012.08.008
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发表时间：
2012-12-16
期刊：
影响因子：
4.5
通讯作者：
Sultana, Sarwat
中科院分区：
文献类型：
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作者：
Khan, Abdul Quaiyoom;Khan, Rehan;Sultana, Sarwat
众所周知，炎症介质的异常产生与大多数毒性表现和包括癌症在内的不同慢性疾病的发生有关。本研究的基本目的是研究大豆异黄酮（SIF）对12-O-十四酰佛波醇-13-乙酸酯（TPA）诱导的皮肤炎症反应的影响，并探讨其分子机制。我们研究了SIF对TPA诱导的小鼠皮肤氧化应激、促炎细胞因子水平、NF-κ B活化、考克斯-2和ki-67表达的保护作用。将动物分为五组I-V（n = 6）。第II、III和IV组以10 nmol/0.2 ml丙酮/动物/天的剂量局部应用TPA，持续2天。在每次TPA给药前30分钟，用SIF 1.0 μ g（D1）和2.0 μ g（D2）局部预处理组III和组IV的动物，而组I和组V分别给予丙酮（0.2 ml）和SIF（D2）。我们发现SIF预处理显著抑制TPA诱导的氧化应激、促炎细胞因子的产生和NF-κ B的活化。抑制考克斯-2和ki-67的表达。组织学结果进一步支持SIF对TPA诱导的皮肤损伤的保护作用。因此，我们的研究结果表明，SW对TPA诱导的皮肤炎症的抑制作用包括抑制促炎细胞因子，减轻氧化应激，激活NF-κ B和考克斯-2的表达。(C)2012爱思唯尔爱尔兰有限公司保留所有权利。
It is well established that aberrant production of inflammatory mediators has been associated with most the toxic manifestations and the genesis of different chronic diseases including cancer. The basic aim of the present study is to investigate the effects of soy isoflavones (SIF) on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced cutaneous inflammatory responses and to explore the underlying molecular mechanisms. We have studied the protective effects of SIF against TPA induced oxidative stress, pro-inflammatory cytokines level, activation of NF-kappa B, expression of COX-2 and ki-67 in mouse skin. Animals were divided into five groups I-V (n = 6). Groups II, III and IV received topical application of TPA at the dose of 10 nmol/0.2 ml of acetone/animal/day, for 2 days. Animals of the groups III and IV were pre-treated with SIF 1.0 mu g (D1) and 2.0 mu g (D2) topically 30 min prior to each TPA administration, while groups I and V were given acetone (0.2 ml) and SIF (D2), respectively. We have found that SIF pretreatment significantly inhibited TPA induced oxidative stress, proinflammatory cytokines production and activation of NF-kappa B. SIF also inhibited the expression of COX-2 and ki-67. Histological findings further supported the protective effects of SIF against TPA-induced cutaneous damage. Thus, our results suggest that inhibitory effect of SW on TPA-induced cutaneous inflammation includes inhibition of proinflammatory cytokines, attenuation of oxidative stress, activation of NF-kappa B and expression of COX-2. (C) 2012 Elsevier Ireland Ltd. All rights reserved.