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首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Attenuation of intestinal ischemia/reperfusion injury with sodium nitroprusside: studies on mitochondrial function and lipid changes
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Attenuation of intestinal ischemia/reperfusion injury with sodium nitroprusside: studies on mitochondrial function and lipid changes

机译:硝普钠减缓肠道缺血/再灌注损伤:线粒体功能和脂质变化的研究

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摘要

Reactive oxygen species have been implicated in cellular injury during ischemia/reperfusion (I/R). Mitochondria are one of the main targets of oxygen free radicals and damage to this organelle leads to cell death. Reports suggest that nitric oxide (NO) may offer protection from damage during I/R. This study has looked at the functional changes and lipid alteration to mitochondria during intestinal I/R and the protection offered by NO. It was observed that I/R of the intestine is associated with functional alterations in the mitochondria as suggested by MTT reduction, respiratory control ratio and mitochondrial swelling. Mitochondrial lipid changes suggestive of activation of phospholipase A_2 and phospholipase D were also seen after (I/R) mediated injury. These changes were prevented by the simultaneous presence of a NO donor in the lumen of the intestine. These studies have suggested that structural and functional alterations of mitochondria are prominent features of I/R injury to the intestine which can be ameliorated by NO.
机译:在缺血/再灌注(I / R)过程中,活性氧物质与细胞损伤有关。线粒体是氧自由基的主要靶标之一,对该细胞器的损害会导致细胞死亡。报告表明,一氧化氮(NO)可以在I / R期间提供保护,使其免受损坏。这项研究研究了肠道I / R期间线粒体的功能变化和脂质变化以及NO的保护作用。观察到肠道的I / R与线粒体功能改变有关,如MTT降低,呼吸控制率和线粒体肿胀所暗示的。 (I / R)介导的损伤后还可见线粒体脂质变化,提示磷脂酶A_2和磷脂酶D活化。在肠腔中同时存在NO供体可防止这些变化。这些研究表明,线粒体的结构和功能改变是肠道I / R损伤的显着特征,而NO可以减轻它。

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