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首页> 外文期刊>The Journal of Nutritional Biochemistry >Resveratrol counteracts gallic acid-induced down-regulation of gap-junction intercellular communication.
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Resveratrol counteracts gallic acid-induced down-regulation of gap-junction intercellular communication.

机译：白藜芦醇抵消了没食子酸诱导的间隙连接细胞间通讯的下调。

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摘要

Since reactive oxygen species (ROS) play a key role in carcinogenesis, many studies have focused on the chemopreventive activities of naturally occurring antioxidants. However, the possibility that different antioxidants in food exert opposing effects on carcinogenesis has not been adequately investigated. Gap-junction intercellular communication (GJIC), which is strongly related to carcinogenesis (particularly the tumor promotion stage), may be a suitable model for investigating the tumor-promoting and antitumor-promoting effects of phytochemicals. The present study investigated the possible combined effects of resveratrol and gallic acid (GA), which are major antioxidants in red wine, on GJIC in WB-F344 rat liver epithelial (RLE) cells. GA at 100 muM, but not resveratrol, inhibited GJIC and generated hydrogen peroxide. The GA-induced inhibition of GJIC was recovered by resveratrol, but only partially recovered by catalase. Resveratrol did not attenuate GA-induced generation of hydrogen peroxide, but it did block GA-induced phosphorylation of connexin 43 (Cx43), a key modulator of GJIC. Furthermore, resveratrol down-regulated GA-induced phosphorylation of extracellular signal-regulated kinase (ERK)1/2, one of the critical regulators of Cx43. However, catalase partially blocked the GA-induced phosphorylation of Cx43 and ERK1/2. Collectively, these findings suggest that the combined effects of red wine phenolic phytochemicals on GJIC and antioxidants differ in ROS-mediated carcinogenesis depending on their dosages and structures. All rights reserved, Elsevier.
机译：由于活性氧（ROS）在致癌过程中起着关键作用，因此许多研究都集中在天然抗氧化剂的化学预防活性上。然而，尚未充分研究食物中不同抗氧化剂对癌变产生相反作用的可能性。与致癌作用（特别是肿瘤促进阶段）密切相关的间隙连接细胞间通讯（GJIC）可能是研究植物化学物质促进肿瘤和促进肿瘤作用的合适模型。本研究调查了白藜芦醇和没食子酸（GA）（它们是红酒中的主要抗氧化剂）对WB-F344大鼠肝上皮（RLE）细胞中GJIC的可能的联合作用。浓度为100μM的GA，但没有白藜芦醇，抑制GJIC并生成过氧化氢。 GA诱导的GJIC抑制作用可通过白藜芦醇恢复，但只能通过过氧化氢酶部分恢复。白藜芦醇不会减弱GA诱导的过氧化氢的生成，但确实可以阻断GA诱导的GJIC关键调节剂连接蛋白43（Cx43）的磷酸化。此外，白藜芦醇下调GA诱导的细胞外信号调节激酶（ERK）1/2的磷酸化，Cx43的关键调节剂之一。但是，过氧化氢酶部分阻断了GA诱导的Cx43和ERK1 / 2的磷酸化。总体而言，这些发现表明，红酒酚类植物化学物质对GJIC和抗氧化剂的综合作用在ROS介导的致癌作用方面有所不同，具体取决于其剂量和结构。保留所有权利，Elsevier。

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