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肿瘤坏死因子α可增强中性粒细胞在体外介导的软骨损伤。

Neutrophil-mediated cartilage injury in vitro is enhanced by tumour necrosis factor alpha.

作者信息

Kowanko I C, Bates E J, Ferrante A

机构信息

Department of Immunology, Adelaide Children's Hospital, South Australia.

出版信息

Rheumatol Int. 1990;10(2):85-90. doi: 10.1007/BF02274789.

Abstract

Neutrophil functions relevant to tissue damage are altered by cytokines such as tumour necrosis factor alpha (cachectin, TNF alpha), known to be present in inflammatory foci. In this study we examined the effect of TNF alpha on neutrophil-mediated cartilage damage in vitro. Human neutrophils were able to injure both human and bovine articular cartilage slices by degrading proteoglycan and inhibiting its synthesis. Recombinant human TNF alpha enhanced neutrophil-mediated degradation of proteoglycan, even when neutrophils were preincubated with TNF alpha and washed before incubating with cartilage. TNF alpha alone degraded proteoglycan and inhibited its synthesis. Neutrophil-mediated inhibition of proteoglycan biosynthesis was increased after incubating cartilage together with neutrophils and TNF alpha, but was unaltered when neutrophils were preincubated with TNF alpha. We conclude that TNF alpha enhances neutrophil injury to articular cartilage.

摘要

与组织损伤相关的中性粒细胞功能会被细胞因子改变,如肿瘤坏死因子α(恶病质素,TNFα),已知其存在于炎症病灶中。在本研究中,我们在体外检测了TNFα对中性粒细胞介导的软骨损伤的影响。人类中性粒细胞能够通过降解蛋白聚糖并抑制其合成来损伤人类和牛的关节软骨切片。重组人TNFα增强了中性粒细胞介导的蛋白聚糖降解,即使中性粒细胞在与软骨孵育前先用TNFα预孵育并洗涤过。单独的TNFα会降解蛋白聚糖并抑制其合成。将软骨与中性粒细胞和TNFα一起孵育后,中性粒细胞介导的蛋白聚糖生物合成抑制作用增强,但当中性粒细胞先用TNFα预孵育时,该抑制作用未改变。我们得出结论,TNFα增强了中性粒细胞对关节软骨的损伤。

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