Cytoprotective effect of epigallocatechin-3-gallate against deoxynivalenol-induced toxicity through anti-oxidative and anti-inflammatory mechanisms in HT-29 cells

Cytoprotective effect of epigallocatechin-3-gallate against deoxynivalenol-induced toxicity through anti-oxidative and anti-inflammatory mechanisms in HT-29 cells
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DOI:
10.1016/j.fct.2013.01.042
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发表时间:
2013-06-01
影响因子:
4.3
通讯作者:
Padma, Viswanadha Vijaya
Padma, Viswanadha Vijaya
中科院分区:
农林科学2区
文献类型:
--
作者:
Kalaiselvi, Palaniswamy;Rajashree, Krishnaswamy;Padma, Viswanadha Vijaya

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脱氧雪腐镰刀菌烯醇(DON)是由镰刀菌属产生的真菌毒素,并且已知在细胞中引发促炎反应。暴露于DON的细胞经历凋亡作为关闭炎症的机制。在这项研究中,我们测试了绿色茶多酚表没食子儿茶素3-没食子酸酯(EGCG)的细胞保护作用,在HT-29细胞中的DON诱导的毒性。EGCG以剂量-反应方式阻止DON诱导的HT-29细胞毒性。即使是最低浓度(5 μ M)的EGCG也显示出对所尝试的最高浓度(3.38 μ M = 1000 ng/ml)的DON的保护作用。我们的研究还表明,DON在HT 29细胞中的IC 20值为250 ng/ml,用20 μ M EGCG预处理产生99%的细胞活力。EGCG还保护氧化应激,上调核因子-κ B(NF-κ B B)、环氧合酶-2(考克斯-2)和caspase-3激活的细胞凋亡。这些结果表明,表没食子儿茶素没食子酸酯作为细胞保护剂对DON诱导的毒性。(C)2013爱思唯尔有限公司保留所有权利。
Deoxynivalenol (DON) is a mycotoxin produced by Fusarium sp., and is known to elicit pro-inflammatory responses in the cell. The cells exposed to DON undergo apoptosis as a mechanism to shut down the inflammation. In this study, we tested the cytoprotective effect of the green tea polyphenol epigallocatechin 3-gallate (EGCG) on DON-induced toxicity in HT-29 cells. EGCG prevented DON-induced cytotoxicity to HT-29 cells in a dose-response manner. Even the lowest concentration (5 mu M) of EGCG showed protection against the highest concentration of DON tried (3.38 mu M = 1000 ng/ml). Our study also demonstrates that IC20 value of DON in HT 29 cells were 250 ng/ml and pre-treatment with 20 mu M EGCG yielded 99% cell viability. EGCG also protected against oxidative stress, up regulation of nuclear factor-kB (NF-kappa B), cyclooxygenase-2 (COX-2) and caspase-3 activated apoptosis. These results suggest that EGCG acts as cytoprotective agent against DON-induced toxicity. (C) 2013 Elsevier Ltd. All rights reserved.