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首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >Mitochondrial bioenergetics, uncoupling protein-2 activity, and reactive oxygen species production in the small intestine of a TNBS-induced colitis rat model
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Mitochondrial bioenergetics, uncoupling protein-2 activity, and reactive oxygen species production in the small intestine of a TNBS-induced colitis rat model

机译：线粒体生物植物，非偶像蛋白-2活性，以及TNBS诱导的结肠炎大鼠模型的小肠中的活性氧物种生产

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Inflammatory bowel disease (IBD) is often associated with a decrease in energy-dependent nutrient uptake across the jejunum that serves as the main site for absorption in the small intestine. This association has prompted us to investigate the bioenergetics underlying the alterations in jejunal absorption in 2,4,6-trinitrobenzenesulfonic acid-induced colitis in rats. We have found that mitochondrial oxygen consumption did not change in state 2 and state 3 respirations but showed an increase in state 4 respiration indicating a decrease in the respiratory control ratio of jejunal mitochondria during the peak of inflammation. This decrease in the coupling state was found to be guanosine diphosphate-sensitive, hence, implicating the involvement of uncoupling protein-2 (UCP2). Furthermore, the study has reported that the production of reactive oxygen species (ROS), known to be activators of UCP2, correlated negatively with UCP2 activity. Thus, we suggest that ROS production in the jejunum might be activating UCP2 which has an antioxidant activity, and that uncoupling of the mitochondria decreases the efficiency of energy production, leading to a decrease in energy-dependent nutrient absorption. Hence, this study is the first to account for an involvement of energy production and a role for UCP2 in the absorptive abnormalities of the small intestine in animal models of colitis.
机译：炎症性肠病（IBD）通常与杂志中的能量依赖性营养吸收的降低有关，其作为小肠中吸收的主要部位。该协会促使我们探讨了在大鼠2,4,6-三硝基苯磺酸诱导的结肠炎中的Jejunal吸收的改变的生物终端。我们发现线粒体氧消耗在状态2和状态3呼吸中没有变化，但显示出状态4呼吸的增加，表明在炎症的峰值期间Jejunal线粒体的呼吸控制比率降低。发现偶联状态的这种降低是鸟氨酸二磷酸敏感性，因此暗示了非偶联蛋白-2（UCP2）的累积。此外，该研究报告说，已知是UCP2的活性剂的活性氧物质（ROS）的产生与UCP2活性负相关。因此，我们建议在Jejunum中的ROS产生可能是激活具有抗氧化活性的UCP2，并且线粒体的解耦降低了能量产生的效率，导致能量依赖性营养吸收降低。因此，本研究是第一个涉及能源生产的参与和UCP2在结肠炎动物模型中小肠的吸收异常中的作用。

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