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、ROS是血管疾病各种病理生理过程的重要介质。此外，NO与超氧阴离子(O^&lt；2-&gt；)相互作用形成的过氧亚硝酸盐可引起蛋白质的组织损伤，包括腹膜。观察高糖(HG组，214 mM)对体外培养的大鼠间皮细胞(MC)的影响。在MC中表达nNOS和iNOSmRNAs，但未检测到eNOS mRNA。此外，暴露于HG后，这些mRNA的合成也增加，随后MC产生的ROS比对照组多，但没有检测到增加NO的产生。四氢生物蝶呤(BH4)抑制了HG条件下ROS的产生。这些结果表明，高糖可促进ROS的产生，而NOS解偶联可抑制ROS的产生。制备腹膜炎模型大鼠。通过…揭示了NOSS的定位多采用免疫组织化学染色方法。对照组大鼠MC中nNOS表达较弱，而本模型大鼠MC中nNOS表达较强。证实iNOS和nNOS在该模型的浸润性细胞中的存在。这些结果证实了NOS异构体的上调，然而，ROS减少了生物可利用的NO。NO和ROS的失衡可能导致腹膜损伤。铁代谢异常在腹膜氧化性损伤发生发展中的作用本研究探讨了铁代谢异常在腹膜氧化性损伤发生发展中的作用。制备腹膜炎模型大鼠。免疫组织化学染色显示铁、铁蛋白、8-羟基脱氧鸟苷(8-OHdG：氧化DNA损伤的指示物)和脂质过氧化(4-羟基壬烯醛：4-HNE)的定位。证实了该模型中浸润性细胞中铁的存在。此外，在这些大鼠的腹膜间皮细胞和血管壁中也检测到了8-OHdG，4-HNE免疫反应性增加。此外，还对50例硬化性腹膜炎患者的腹膜活检标本进行了检验。健康对照组未检出铁。而硬化性腹膜炎患者的腹膜下皮下区和血管壁有较强的染色。腹膜炎的浸润性细胞中铁的存在被证实。铁代谢异常产生的氧自由基参与了腹膜或腹膜血管的氧化应激，并促进了动脉硬化。较少

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