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首页> 外文期刊>Archives of the Balkan Medical Union : >Pathogenetic features of lipid and protein peroxide oxidation due to experimental acute ne-crotizing pancreatitis
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Pathogenetic features of lipid and protein peroxide oxidation due to experimental acute ne-crotizing pancreatitis

机译:实验性急性坏死性胰腺炎导致脂质和蛋白质过氧化物氧化的致病特征

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摘要

The objective of the study was to research the dynamics of changes in oxidative and reducing systems in the blood and tissues of the pancreas, lungs and liver during the development of acute necrotizing pancreatitis. Material and methods . The experiment involved 63 sexually-mature rabbits “Gray giant”. The degree of oxidative modification of plasma proteins was assessed by the method of I.F. Meshchyshen. The content of malonic aldehyde in the erythrocytes was determined by the method of I. D. Stalna and T.G. Gorishvili. The content of ceruloplasmin in the serum was studied by M.I. Revina method. The level of medium mass molecules was determined by the method of N.I. Gabrielyan. The oxidative modification of proteins in the tissues of the pancreas, liver and lungs was carried out using the histochemical method and original techniques. Results . The development of acute necrotic pancreatitis in the experiment was characterized by an increase in the activity of lipids and proteins in the blood and the oxidative modification of proteins in pancreatocytes, hepatocytes and alveocytes, which is one of the leading mechanisms for their lesion. The growth of the oxidative modification of proteins in the endothelial cells of the pancreas, liver and lungs in the development of acute pancreatitis contributes to the occurrence of endothelial dysfunction, which is the leading factor in the secondary lesions of these organs. Conclusions . Considering the important role of lipoperoxidation and oxidative modification of proteins in the mechanisms of progression of acute necrotic pancreatitis, it is pathogenically grounded to develop new effective methods of systemic and local antioxidant and anti-proteolytic effects.
机译:这项研究的目的是研究急性坏死性胰腺炎发展过程中胰腺,肺和肝脏血液和组织中氧化和还原系统的变化动态。材料与方法 。实验涉及63只性成熟的兔子“灰色巨人”。血浆蛋白的氧化修饰程度通过I.F. Meshchyshen。红血球中丙二醛的含量通过I.D.Stalna和T.G.J.的方法测定。戈里什维利。 M.I. Revina方法。中等质量分子的水平通过N.I.加布里埃良。使用组织化学方法和原始技术对胰腺,肝和肺组织中的蛋白质进行氧化修饰。结果。实验中急性坏死性胰腺炎的发展以血液中脂质和蛋白质的活性增加以及胰腺细胞,肝细胞和肺泡细胞中蛋白质的氧化修饰为特征,这是其病变的主要机制之一。在急性胰腺炎的发展过程中,胰腺,肝和肺的内皮细胞中蛋白质的氧化修饰的增长促进了内皮功能障碍的发生,这是这些器官继发性病变的主要因素。结论。考虑到脂的过氧化和蛋白质的氧化修饰在急性坏死性胰腺炎的发展机制中的重要作用,病因性的基础,以开发新的有效的全身和局部抗氧化剂和抗蛋白水解作用的方法。

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