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在实验性肾小球肾炎中,肾小球巨噬细胞产生活性氧。

Glomerular macrophages produce reactive oxygen species in experimental glomerulonephritis.

作者信息

Boyce N W, Tipping P G, Holdsworth S R

机构信息

Monash University, Department of Medicine, Prince Henry's Hospital, Melbourne, Australia.

出版信息

Kidney Int. 1989 Mar;35(3):778-82. doi: 10.1038/ki.1989.52.

DOI:10.1038/ki.1989.52
PMID:2540375
Abstract

The production of reactive oxygen species by intraglomerular macrophages was assessed in a macrophage dependent model of diffuse proliferative glomerulonephritis in rabbits. Glomerular macrophages were obtained from isolated nephritic glomeruli by short term (60 min) culture. Control macrophage populations were simultaneously obtained from peripheral blood (blood monocytes) and lung lavage fluid (alveolar macrophages). Superoxide anion (O2-), hydrogen peroxide (H2O2) and hydroxyl radical (OH.) production was assessed. Glomerular macrophage production of O2- (48.9 +/- 5.5 nmol/hr/10(6) cells), H2O2 (4.4 +/- 2.5 nmol/hr/10(6) cells) and OH. (57.8 +/- 4.7 U/hr/10(6) cells) was significantly greater than the production of reactive oxygen species seen with control monocyte populations: alveolar macrophages, O2- 9.8 +/- 2.0 nmol/hr/10(6) cells; H2O2 0.6 +/- 0.3 nmol/hr/10(6) cells; OH. 11.0 +/- 1.8 U/hr/10(6) cells; blood monocytes, O2- 8.6 +/- 1.4 nmol/hr/10(6) cells; OH. 9.9 +/- 1.2 U/hr/10(6) cells, (all P less than 0.05 cf. glom macs). Hydrogen peroxide production by blood monocytes (1.6 +/- 0.9 nmol/hr/10(6) cells) was less than glomerular macrophages, however this difference was not statistically significant. The enhanced production of reactive oxygen species by glomerular macrophages in this macrophage dependent model of glomerulonephritis suggests that these mononuclear cells are locally activated within the glomerulus following recruitment from the circulation. Reactive oxygen species production by glomerular macrophages may contribute to their ability to induce glomerular basement membrane injury in this disease.

摘要

在兔弥漫性增殖性肾小球肾炎的巨噬细胞依赖性模型中,评估了肾小球内巨噬细胞产生活性氧的情况。通过短期(60分钟)培养从分离的肾炎性肾小球中获取肾小球巨噬细胞。同时从外周血(血液单核细胞)和肺灌洗液(肺泡巨噬细胞)中获取对照巨噬细胞群体。评估了超氧阴离子(O2-)、过氧化氢(H2O2)和羟自由基(OH.)的产生。肾小球巨噬细胞产生的O2-(48.9±5.5 nmol/小时/10(6)个细胞)、H2O2(4.4±2.5 nmol/小时/10(6)个细胞)和OH.(57.8±4.7 U/小时/10(6)个细胞)显著高于对照单核细胞群体产生活性氧的水平:肺泡巨噬细胞,O2- 9.8±2.0 nmol/小时/10(6)个细胞;H2O2 0.6±0.3 nmol/小时/10(6)个细胞;OH. 11.0±1.8 U/小时/10(6)个细胞;血液单核细胞,O2- 8.6±1.4 nmol/小时/10(6)个细胞;OH. 9.9±1.2 U/小时/10(6)个细胞,(所有P均小于0.05,与肾小球巨噬细胞相比)。血液单核细胞产生的过氧化氢(1.6±0.9 nmol/小时/10(6)个细胞)低于肾小球巨噬细胞,然而这种差异无统计学意义。在这种肾小球肾炎的巨噬细胞依赖性模型中,肾小球巨噬细胞产生活性氧增加表明这些单核细胞从循环中募集后在肾小球内被局部激活。肾小球巨噬细胞产生活性氧可能有助于其在该疾病中诱导肾小球基底膜损伤的能力。

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