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首页> 外文期刊>Molecular Carcinogenesis >Butyrate Modulates Antioxidant Enzyme Expression in Malignant and Non-Malignant Human Colon Tissues
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Butyrate Modulates Antioxidant Enzyme Expression in Malignant and Non-Malignant Human Colon Tissues

机译：丁酸酯调节恶性和非恶性人类结肠组织中的抗氧化酶表达。

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The induction of antioxidant enzymes is an important mechanism in colon cancer chemoprevention, but the response of human colon tissue to butyrate, a gut fermentation product derived from dietary fiber, remains largely unknown. Therefore, our study investigated the effect of a butyrate treatment on catalase (CAT) and superoxide dismutase (SOD2) in matched human colon tissues of different transformation stages (n = 3-15 in each group) ex vivo. By performing quantitative real-time PCR, Western blot, and spectrophotometric measurements, we found an increase in SOD2 at expression and activity level in colonic adenocarcinomas (mRNA: 1.96-fold; protein: 1.41-fold, activity: 1.8-fold; P < 0.05). No difference was detectable for CAT between normal, adenoma, and carcinoma colon tissues. Treatment of normal colon epithelium (12 h) with a physiologically relevant concentration of butyrate (10mM) resulted in a significant increase (P < 0.05) in CAT mRNA (1.24-fold) and protein (1.39-fold), without affecting the enzymatic activity. Consequently, preliminary experiments failed to show any protective effect of butyrate against H2O2-mediated DNA damage. Despite a significantly lowered SOD2 transcript (0.51-fold, P < 0.01) and, to a lesser extent, protein level (0.86-fold) after butyrate exposure of normal colon cells, the catalytic activity was significantly enhanced (1.19-fold, P < 0.05), suggesting an increased protection against tissue superoxide radicals. In malignant tissues, greater variations in response to butyrate were observed. Furthermore, both enzymes showed an age-dependent decrease in activity in normal colon epithelium (CAT: r = -0.49, P = 0.09; SOD2: r = -0.58, P = 0.049). In conclusion, butyrate exhibited potential antioxidant features ex vivo but cellular consequences need to be investigated more in depth. (C) 2014 Wiley Periodicals, Inc.
机译：抗氧化酶的诱导是结肠癌化学预防的重要机制，但是人类结肠组织对丁酸的反应仍然是未知的，丁酸是膳食纤维的肠道发酵产物。因此，我们的研究调查了丁酸盐处理对不同转化阶段（每组n-15）中匹配的人结肠组织中过氧化氢酶（CAT）和超氧化物歧化酶（SOD2）的影响。通过进行实时定量PCR，蛋白质印迹和分光光度法测量，我们发现结肠腺癌中SOD2在表达和活性水平上有所增加（mRNA：1.96倍;蛋白质：1.41倍，活性：1.8倍; P < 0.05）。正常，腺瘤和结肠癌组织之间的CAT没有差异。用生理学上相关的丁酸浓度（10mM）处理正常结肠上皮（12 h），可使CAT mRNA（1.24倍）和蛋白质（1.39倍）显着增加（P <0.05），而不会影响酶的活性。因此，初步实验未能显示丁酸酯对H2O2介导的DNA损伤的任何保护作用。尽管在正常结肠细胞中丁酸暴露后，SOD2转录显着降低（0.51倍，P <0.01），蛋白质水平降低（0.86倍），但催化活性显着增强（1.19倍，P <0.01）。 0.05），表明针对组织超氧化物自由基的保护作用增强。在恶性组织中，观察到对丁酸酯响应的更大变化。此外，两种酶在正常结肠上皮中均显示出年龄依赖性的活性降低（CAT：r = -0.49，P = 0.09; SOD2：r = -0.58，P = 0.049）。总之，丁酸酯离体表现出潜在的抗氧化剂特性，但细胞后果需要更深入的研究。 （C）2014威利期刊公司

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