首页> 外文期刊>Journal of clinical biochemistry and nutrition. >Qing Dai attenuates nonsteroidal anti-inflammatory drug-induced mitochondrial reactive oxygen species in gastrointestinal epithelial cells
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Qing Dai attenuates nonsteroidal anti-inflammatory drug-induced mitochondrial reactive oxygen species in gastrointestinal epithelial cells

机译:清代减弱胃肠道上皮细胞中非甾体类抗炎药诱导的线粒体反应性氧种类

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Treatments with nonsteroidal anti-inflammatory drugs (NSAIDs) have increased the number of patients with gastrointestinal complications. Qing Dai has been traditionally used in Chinese herbal medicine for various inflammatory diseases such as ulcerative colitis. We previously reported that Qing Dai suppressed inflammations by scavenging reactive oxygen species (ROS) in ulcerative colitis patients. Thus, Qing Dai can attenuate the production of ROS, which play an important role in NSAID-induced gastrointestinal injuries. In this study, we aimed to elucidate whether Qing Dai decreased mitochondrial ROS production in NSAID-treated gastrointestinal cells by examining cellular injury, mitochondrial membrane potentials, and ROS production with specific fluorescent indicators. We also performed electron paramagnetic resonance measurement in isolated mitochondria with a spin-trapping reagent (CYPMPO or DMPO). Treatments with indomethacin and aspirin induced cellular injury and mitochondrial impairment in the gastrointestinal cells. Under these conditions, mitochondrial alterations were observed on electron microscopy. Qing Dai prevented these complications by suppressing ROS production in gastrointestinal cells. These results indicate that Qing Dai attenuated the ROS production from the NSAID-induced mitochondrial alteration in the gastrointestinal epithelial cells. Qing Dai treatment may be considered effective for the prevention NSAID-induced gastrointestinal injury.
机译:非甾体类抗炎药(NSAIDs)的治疗增加了胃肠道并发症的患者人数。青黛传统上已用于中草药治疗各种炎性疾病,例如溃疡性结肠炎。我们先前曾报道,青黛通过清除溃疡性结肠炎患者的活性氧(ROS)来抑制炎症。因此,清代可以减弱ROS的产生,其在NSAID引起的胃肠道损伤中起重要作用。在这项研究中,我们旨在通过检查细胞损伤,线粒体膜电位和具有特定荧光指示剂的ROS来阐明青黛是否降低了经NSAID处理的胃肠道细胞中线粒体ROS的产生。我们还使用自旋捕获剂(CYPMPO或DMPO)在孤立的线粒体中进行了电子顺磁共振测量。消炎痛和阿司匹林的治疗在胃肠道细胞中引起细胞损伤和线粒体损伤。在这些条件下,在电子显微镜下观察到线粒体改变。青黛通过抑制胃肠道细胞中ROS的产生来预防这些并发症。这些结果表明,清代减弱了由NSAID诱导的胃肠道上皮细胞中线粒体改变的ROS产生。清代治疗可能被认为对预防NSAID引起的胃肠道损伤有效。

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