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首页> 外文期刊>The Journal of Nutritional Biochemistry >Catechin protects against ketoprofen-induced oxidative damage of the gastric mucosa by up-regulating Nrf2 in vitro and in vivo.
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Catechin protects against ketoprofen-induced oxidative damage of the gastric mucosa by up-regulating Nrf2 in vitro and in vivo.

机译：儿茶素可通过在体内和体外上调Nrf2来防止酮洛芬引起的胃粘膜氧化损伤。

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摘要

Nonsteroidal anti-inflammatory drugs (NSAIDs), including ketoprofen, are widely used in clinical medicine. However, these drugs may damage the gastrointestinal mucosa. Some reports have suggested that intestinal diseases, such as ulcers, are associated with lipid peroxidation and oxidative damage in the mucosa. Phytochemicals, such as polyphenols, are common dietary antioxidants that possess many beneficial characteristics, such as antioxidant and anti-inflammatory capabilities. The objective of this study was to investigate the protective effects of polyphenols on ketoprofen-induced oxidative damage in the gastrointestinal mucosa. We evaluated the effects of catechin, theaflavin, malvidin, cyanidin and apigenin on the activity of antioxidant enzymes in human intestinal-407 (Int-407) cells and rat primary gastric cells treated with ketoprofen. The results indicated that catechin significantly (P < .05) decreased the levels of lipid peroxidation (40.5%) and reactive oxygen species (30.0%), and increased the activity of intracellular antioxidant enzymes glutathione peroxidase, glutathione reductase and total sulfhydryl groups. More importantly, the treatment of Sprague-Dawley rats with catechin (35 mg/kg/day) prior to the administration of ketoprofen (50 mg/kg/day) successfully inhibited oxidative damage and reversed the impairment of the antioxidant system in the intestinal mucosa. Western blot analysis revealed that catechin stimulated a time-dependent increase in both the nuclear factor erythroid 2-related factor 2 and total heme oxygenase-1 protein expression in Int-407 cells. These results suggest that catechin may have a protective effect on gastrointestinal ulcers. All rights reserved, Elsevier.
机译：包括酮洛芬在内的非甾体抗炎药（NSAID）被广泛用于临床医学。但是，这些药物可能会损害胃肠道粘膜。一些报告表明肠道疾病，例如溃疡，与粘膜脂质过氧化和氧化损伤有关。植物化学物质（例如多酚）是常见的饮食抗氧化剂，具有许多有益的特性，例如抗氧化剂和抗炎能力。这项研究的目的是研究多酚对酮洛芬引起的胃肠道粘膜氧化损伤的保护作用。我们评估了儿茶素，茶黄素，malvidin，花青素和芹菜素对人肠407（Int-407）细胞和用酮洛芬治疗的大鼠原代胃细胞中抗氧化酶活性的影响。结果表明，儿茶素显着（P <.05）降低了脂质过氧化水平（40.5％）和活性氧种类（30.0％），并增加了细胞内抗氧化酶谷胱甘肽过氧化物酶，谷胱甘肽还原酶和总巯基的活性。更重要的是，在给予酮洛芬（50 mg / kg /天）之前用儿茶素（35 mg / kg /天）治疗Sprague-Dawley大鼠成功抑制了氧化损伤并逆转了肠粘膜中抗氧化系统的损伤。 。蛋白质印迹分析表明，儿茶素刺激Int-407细胞中核因子红系2相关因子2和总血红素加氧酶1蛋白表达随时间的增加。这些结果表明儿茶素可能对胃肠道溃疡具有保护作用。保留所有权利，Elsevier。

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