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NADPH oxidase is involved in ischaemia/reperfusion-induced damage in rat gastric mucosa via ROS production – Role of NADPH oxidase in rat stomachs

机译:NADPH氧化酶通过产生ROS参与缺血/再灌注引起的大鼠胃粘膜损伤– NADPH氧化酶在大鼠胃中的作用

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摘要

In the process of the oxygen reduction, NADPH oxidase is the enzyme that produces superoxide anion, which subsequently produces reactive oxygen species (ROS) and causes damage in various tissues and microorganisms. NADPH oxidase is demonstrated to exist in several types of cells such as endothelial cells and vascular smooth muscle cells. In the present study, we examined the role of NADPH oxidase in ischaemia/reperfusion (I/R)-induced damage in the rat gastric mucosa. Male SD rats were used after 18 h fasting. Under urethane anaesthesia, the stomach was mounted in an ex-vivo chamber, applied with 100 mM HCl, and a catheter was passed through the left femoral vein. To produce I/R, 4 mL of blood was removed at for 30 min, and then reperfused. DPI was given i.v. 10 min before reperfusion. The combination of ischaemia and reperfusion produced haemorrhagic damage in the rat gastric mucosa. The damage was attenuated by pretreatment of DPI. I/R increased microvascular permeability, the amount of H2O2 and NADPH oxidase activity in the stomach. These increases were suppressed by pretreatment of DPI. As to the presence of a subunit of NADPH oxidase, we detected protein level of p47phox in the gastric mucosa. In conclusion, these results showed that ROS production via NADPH oxidase activity is involved in the pathogenic mechanism of I/R damage in the rat stomach and suggested that activation of NADPH oxidase and the associated ROS product could be a potential target in the gastrointestinal mucosal damage.
机译:在氧还原过程中,NADPH氧化酶是产生超氧阴离子的酶,随后会产生活性氧(ROS),并在各种组织和微生物中造成损害。 NADPH氧化酶被证明存在于几种类型的细胞中,例如内皮细胞和血管平滑肌细胞。在本研究中,我们检查了NADPH氧化酶在缺血/再灌注(I / R)诱导的大鼠胃粘膜损伤中的作用。禁食18小时后使用雄性SD大鼠。在氨基甲酸乙酯麻醉下,将胃安装在离体室中,并用100 mM HCl施加,然后将导管穿过左股静脉。为了产生I / R,在30分钟内取出4 mL血液,然后再灌注。静脉注射DPI再灌注前10分钟。缺血和再灌注的结合在大鼠胃粘膜中产生出血性损害。 DPI预处理可减轻损害。 I / R增加了胃中微血管的通透性,H2 O2 的含量和NADPH氧化酶的活性。 DPI的预处理抑制了这些增加。关于NADPH氧化酶亚基的存在,我们检测了胃粘膜中p47phox 的蛋白水平。总之,这些结果表明,通过NADPH氧化酶活性产生的ROS参与了大鼠胃I / R损伤的发病机制,并表明NADPH氧化酶和相关ROS产物的激活可能是胃肠道黏膜损伤的潜在靶标。 。

著录项

  • 来源
    《Inflammopharmacology》 |2007年第6期|278-281|共4页
  • 作者单位

    Department of Pharmacotherapeutics Doshisha Women’s College of Liberal Arts Kodo Kyotanabe Kyoto 610-0395 Japan;

    Department of Pharmacotherapeutics Doshisha Women’s College of Liberal Arts Kodo Kyotanabe Kyoto 610-0395 Japan;

    Department of Pharmacotherapeutics Doshisha Women’s College of Liberal Arts Kodo Kyotanabe Kyoto 610-0395 Japan;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    Ischaemia/reperfusion; Gastric damage; Reactive oxygen species; NADPH oxidase;

    机译:缺血/再灌注;胃损伤;活性氧;NADPH氧化酶;

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