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表儿茶素通过体外和体内上调 Nrf2 来防止酮洛芬引起的胃黏膜氧化损伤。

Catechin protects against ketoprofen-induced oxidative damage of the gastric mucosa by up-regulating Nrf2 in vitro and in vivo.

机构信息

Department of Food Science and Biotechnology, National Chung Hsing University, Taichung 402, Taiwan.

出版信息

J Nutr Biochem. 2013 Feb;24(2):475-83. doi: 10.1016/j.jnutbio.2012.01.010. Epub 2012 Jun 15.

DOI:10.1016/j.jnutbio.2012.01.010
PMID:22704780
Abstract

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.

摘要

非甾体抗炎药(NSAIDs),包括酮洛芬,广泛应用于临床医学。然而,这些药物可能会损伤胃肠道黏膜。一些报告表明,肠道疾病,如溃疡,与黏膜的脂质过氧化和氧化损伤有关。植物化学物质,如多酚,是常见的膳食抗氧化剂,具有许多有益的特性,如抗氧化和抗炎能力。本研究旨在探讨多酚对酮洛芬诱导的胃肠道黏膜氧化损伤的保护作用。我们评估了儿茶素、茶黄素、矢车菊素、花青素和芹菜素对酮洛芬处理的人肠-407(Int-407)细胞和大鼠原代胃细胞中抗氧化酶活性的影响。结果表明,儿茶素显著(P<.05)降低了脂质过氧化(40.5%)和活性氧(30.0%)的水平,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/d)之前,用儿茶素(35 mg/kg/d)对 Sprague-Dawley 大鼠进行预处理成功抑制了氧化损伤,并逆转了肠道黏膜抗氧化系统的损伤。Western blot 分析显示,儿茶素刺激 Int-407 细胞中核因子红细胞 2 相关因子 2 和总血红素加氧酶-1 蛋白表达的时间依赖性增加。这些结果表明儿茶素可能对胃肠道溃疡具有保护作用。

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