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[氧自由基在肾小球肾炎发病机制中的作用]

[The role of oxygen radicals in the pathogenesis of glomerulonephritis].

作者信息

Zima T, Tesar V, Stípek S, Nĕmecek K, Pláteník J

机构信息

I. Ustav lékarské chemie a biochemie I. LF UK a VFN, Praha.

出版信息

Cas Lek Cesk. 1995 Nov 15;134(22):716-9.

PMID:8599808
Abstract

In the pathogenesis of glomerulonephritis, acute renal failure, pyelonephritis and other diseases of the kidneys oxygen radicals are involved. Some types of glomerulonephritis are characterized by infiltration of the glomeruli by neutrophils and monocytes which can form oxygen radicals (superoxide, hydrogen peroxide). The increased amount of cAMP in glomeruli can be due to oxygen radicals. Cyclic nucleotides modulate the inflammatory or immune response in glomerular disease and play a part in the action of local mediators of the inflammation. Oxygen radicals act as second messenger for the activation of cytokines via NF-kappaB transcription factor, they stimulate the formation of TNF-alpha, IL-1, IL-6 and influence the expression of monocyte-specific cytokines (CSF-1 and MCP-1). Radicals formed by the system myeloperoxidase--hydrogen peroxide--halogen derivatives activate proteolytic enzymes (proteinases) which break down collagen and other components of the extracellular matrix present in the basal membrane of glomeruli and in the mesangium. Oxygen radicals and proteinases can cause and amplify glomerular damage. Glucocorticoid administration leads to an increased activity of endogenous antioxidant enzymes in the glomerulus and reduced the of lipid peroxidation.

摘要

在肾小球肾炎、急性肾衰竭、肾盂肾炎及其他肾脏疾病的发病机制中,氧自由基参与其中。某些类型的肾小球肾炎的特征是中性粒细胞和单核细胞浸润肾小球,这些细胞可形成氧自由基(超氧化物、过氧化氢)。肾小球中cAMP量的增加可能归因于氧自由基。环核苷酸调节肾小球疾病中的炎症或免疫反应,并在炎症局部介质的作用中发挥作用。氧自由基作为通过NF-κB转录因子激活细胞因子的第二信使,刺激肿瘤坏死因子-α、白细胞介素-1、白细胞介素-6的形成,并影响单核细胞特异性细胞因子(集落刺激因子-1和单核细胞趋化蛋白-1)的表达。髓过氧化物酶-过氧化氢-卤素衍生物系统形成的自由基激活蛋白水解酶,这些酶分解肾小球基底膜和系膜中存在的细胞外基质的胶原蛋白和其他成分。氧自由基和蛋白水解酶可导致并放大肾小球损伤。给予糖皮质激素会导致肾小球内源性抗氧化酶活性增加,并减少脂质过氧化。

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