The implication of NO, R0S and their interaction in the pathogenesis of peritoneal injury

NO、ROS及其相互作用在腹膜损伤发病机制中的意义NO和ROS是血管疾病各种病理生理过程的重要介质。此外，一氧化氮与超氧阴离子（O^<2->）相互作用形成的过氧亚硝酸盐可引起包括腹膜在内的蛋白质的组织损伤。研究了高葡萄糖浓度（HG组，214mM）对大鼠培养间皮细胞（MC）的影响。MC中表达了nNOS和iNOS mRNA，但未检测到eNOS mRNA。此外，暴露于HG后，这些mRNA的合成也增加了，随后，MC产生了比对照组更多的ROS，但没有检测到NO的增加。四氢生物蝶呤（BH4）抑制HG条件下ROS的产生。这些结果表明，在高糖条件下，ROS生成加速，NOS解偶联减少。制备腹膜炎模型大鼠。免疫组化染色法显示NOSs的定位。nNOS在对照组大鼠的MC中呈弱染色，而在该模型中呈强染色。证实了该模型浸润细胞中iNOS和nNOS的存在。这些结果证实了一氧化氮异构体的上调，但活性氧减少了生物可利用的一氧化氮。一氧化氮和活性氧失衡可引起腹膜损伤。铁代谢异常在腹膜氧化损伤发生中的作用本研究探讨了铁代谢异常在腹膜氧化损伤发生中的作用。制备腹膜炎模型大鼠。免疫组化染色法显示铁、铁蛋白、8-羟基脱氧鸟苷（8-OHdG：一种DNA氧化损伤指标）和脂质过氧化（4-羟基壬烯醛：4-HNE）的定位。该模型证实了铁在浸润细胞中的存在。在这些大鼠的间皮细胞和血管壁中检测到8-OhdG，并增加了4-HNE的免疫反应性。此外，我们还对50例硬化性腹膜炎患者的腹膜活检标本进行了检查。在健康对照组中未检测到铁。然而，在硬化性腹膜炎患者的间皮下区和血管壁观察到强烈的染色。证实了腹膜炎浸润细胞中铁的存在。铁代谢异常产生的氧自由基参与腹膜或腹膜血管的氧化应激，促进动脉硬化。少

The implication of NO, ROS and their interaction in the pathogenesis of peritoneal injuryNO and ROS are important mediators of various pathophysiological processes in vascular diseases. In addition, peroxynitrite formed by the interaction of NO and superoxide anion (O^<2->) can cause tissue damage of proteins, including the peritoneal membrane. The effect of a high glucose concentration (HG group, 214mM) on rat culture mesothelial cells (MC) was investigated. nNOS and iNOS mRNAs were expressed in the MC, however, eNOS mRNA was not detected. Furthermore, upon exposure to HG, these mRNA synthesis also increased, Subsequently, the MC produced more ROS than the control, however, increased production of NO was not detected. Tetrahydrobiopterin (BH4) was suppressed ROS production in HG condition. These results suggest that the accelerated ROS production and diminished by NOS uncoupling were revealed under High glucose. Peritonitis model rats were prepared. Localization of NOSs was revealed b … More y immunohistochemical staining method. nNOS was weakly detected in the MC of the control rats, however, strong staining was in this model. The presence of iNOS and nNOS in infiltrative cells in this model was confirmed. These results confirmed the up-regulation of NOS isoform, however, diminished bioavailable NO by ROS. The unbalance of NO and ROS may cause the peritoneal injury.The Role Of Abnormal Iron Metabolism In The Development Of Oxidative Peritoneal InjuryThis study examined the role of abnormal iron metabolism in causing the development of oxidative peritoneal injury. Peritonitis model rats were prepared. Localisation of iron, ferritin, 8-hydroxydeoxyguanosine (8-OHdG : an indicator of oxidative DNA damage) and lipid peroxidation (4-hydroxynonenal : 4-HNE) was revealed by the immunohistochemical staining method. The presence of iron in infiltrative cells in this model was confirmed. Also, 8-OhdG was detected in the mesothelial cells and vascular walls of these rats, as was increased 4-HNE immnoreactivity. Furthermore, human peritoneal biopsy specimens from fifty patients with sclerosing peritonitis were exmained. Iron was not detected in the healthy control group. However, strong staining was observed in the submesothelial areas and vascular walls of the patients with sclerosing peritonitis. The presence of iron in infiltrative cells in peritonitis was confirmed. The oxygen radical generated by the abnormalities in iron metabolism is involved in oxidative stress in the peritoneum or in peritoneal vessels, and in promotion of arteriosclerosis. Less