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首页> 外文期刊>Life sciences >Upregulation of heme oxygenase-1 by epigallocatechin-3-gallate via the phosphatidylinositol 3-kinase/Akt and ERK pathways
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Upregulation of heme oxygenase-1 by epigallocatechin-3-gallate via the phosphatidylinositol 3-kinase/Akt and ERK pathways

机译：表没食子儿茶素-3-没食子酸酯通过磷脂酰肌醇3-激酶/ Akt和ERK途径上调血红素加氧酶-1

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摘要

Heme oxygenase-1 (HO-1) is a cytoprotective enzyme activated by various phytochemicals and we examined the ability of Epigallocatechin-3-gallate (EGCG), the major constituent of green tea, to upregulate HO-1 expression in endothelial cells (ECs). We demonstrate that EGCG induces HO-1 expression in a concentration- and time-dependent manner. Furthermore, EGCG-mediated HO-1 induction was abrogated in the presence of actinomycin D and cycloheximide, indicating that this upregulation of HO-1 occurred at the transcriptional level. EGCG also upregulates Nrf2 levels in nuclear extracts and increases ARE-luciferase activity. Furthermore, EGCG is the most potent inducer of HO-1 expression of the different green tea constituents that we analyzed, but had no detectable cytotoxic effects over the 25-100 mu M dosage range. The inhibition of intracellular ROS production by N-acetylcysteine (NAC), glutathione (GSH), superoxide dismutase (SOD), catalase and the mitochondrial complex I inhibitor, rotenone, results in a decrease in EGCG-dependent HO-1 expression. In addition, we determined that tyrosine kinase is involved in EGCG induction of HO-1 as this is abrogated by genistein. ECs treated with EGCG exhibit activation of Akt and ERK1/2. In addition, pharmacological inhibitors of phosphatidylinositol 3-kinase and MEK1/2, which are upstream of Akt and ERK1/2, respectively, attenuate EGCG-induced HO-1 expression. On the other hand, pretreatment of these cells with EGCG exerts significant cytoprotective effects against H2O2, suggesting that the induction of HO-1 is an important component in the protection against oxidative stress. Hence, EGCG is a novel phytochemical inducer of HO-1 expression and we further identify the principal underlying mechanisms involved in this process. (c) 2005 Elsevier Inc. All rights reserved.
机译：血红素加氧酶-1（HO-1）是一种被多种植物化学物质激活的细胞保护酶，我们研究了绿茶的主要成分Epigallocatechin-3-gallate（EGCG）上调内皮细胞（ECs）HO-1表达的能力。 ）。我们证明，EGCG以浓度和时间依赖性方式诱导HO-1表达。此外，在放线菌素D和环己酰亚胺的存在下，EGCG介导的HO-1诱导被取消，这表明HO-1的这种上调发生在转录水平。 EGCG还可以上调核提取物中的Nrf2水平，并提高ARE荧光素酶的活性。此外，EGCG是我们分析过的不同绿茶成分中HO-1表达最有效的诱导剂，但在25-100μM剂量范围内没有可检测到的细胞毒性作用。 N-乙酰半胱氨酸（NAC），谷胱甘肽（GSH），超氧化物歧化酶（SOD），过氧化氢酶和线粒体复合物I抑制剂鱼藤酮对细胞内ROS产生的抑制作用导致EGCG依赖性HO-1表达降低。此外，我们确定酪氨酸激酶与HO-1的EGCG诱导有关，因为它已被染料木黄酮废除。用EGCG处理的EC表现出Akt和ERK1 / 2的激活。此外，分别位于Akt和ERK1 / 2上游的磷脂酰肌醇3-激酶和MEK1 / 2的药理抑制剂会减弱EGCG诱导的HO-1表达。另一方面，用EGCG预处理这些细胞对H2O2具有重要的细胞保护作用，这表明HO-1的诱导是抗氧化应激的重要组成部分。因此，EGCG是HO-1表达的新型植物化学诱导剂，我们进一步确定了该过程涉及的主要潜在机制。 （c）2005 Elsevier Inc.保留所有权利。

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