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小鼠抗原诱导性和酵母聚糖诱导性关节炎:体内软骨蛋白聚糖合成及软骨细胞死亡的研究

Antigen-induced and zymosan-induced arthritis in mice: studies on in vivo cartilage proteoglycan synthesis and chondrocyte death.

作者信息

van den Berg W B, Kruijsen M W, van de Putte L B, van Beusekom H J, van der Sluis-van der Pol M, Zwarts W A

出版信息

Br J Exp Pathol. 1981 Jun;62(3):308-16.

Abstract

The influence of joint inflammation on patellar hyaline articular cartilage was studied in mice. Antigen-induced and zymosan-induced arthritis were used as models for immunologically and non-immunologically induced joint inflammation. The contribution of newly formed proteoglycan to the cartilage proteoglycan content, as measured by labelling of the cartilage after i.v. administration of 35S-sulphate, was decreased in parallel with the severity of inflammation during both zymosan-induced and antigen-induced arthritis. The decreased 35S content of the cartilage was due to inhibition of synthesis rather than breakdown of newly synthesized proteoglycan, since no accelerated release of 35S from arthritic cartilage could be demonstrated in vitro. Antigen-induced arthritis was associated with progressive chondrocyte damage. Loss of chondrocytes was consistently found in the central part of the patella, without nearby presence of pannus. It would appear that, in addition to enzymatic breakdown of cartilage, other phenomena are important in cartilage destruction: inhibition of proteoglycan synthesis and chondrocyte death, apparently unrelated to pannus formation.

摘要

在小鼠中研究了关节炎症对髌透明关节软骨的影响。抗原诱导性关节炎和酵母聚糖诱导性关节炎被用作免疫性和非免疫性诱导关节炎症的模型。静脉注射35S-硫酸盐后对软骨进行标记,以此测量新形成的蛋白聚糖对软骨蛋白聚糖含量的贡献,在酵母聚糖诱导性关节炎和抗原诱导性关节炎期间,该贡献均与炎症严重程度平行降低。软骨中35S含量的降低是由于新合成蛋白聚糖的合成受到抑制,而非分解,因为在体外未证明来自关节炎软骨的35S有加速释放。抗原诱导性关节炎与软骨细胞的进行性损伤有关。在髌骨中央部分始终发现软骨细胞缺失,且附近没有血管翳。看来,除了软骨的酶促分解外,其他现象在软骨破坏中也很重要:蛋白聚糖合成的抑制和软骨细胞死亡,显然与血管翳形成无关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e920/2041692/e3d0712c9f0b/brjexppathol00111-0100-a.jpg

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