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电荷与关节炎症。用竞争性聚阳离子抑制阳离子牛血清白蛋白诱导的关节炎

Electrical charge and joint inflammation. Suppression of cationic aBSA-induced arthritis with a competitive polycation.

作者信息

van den Berg W B, Joosten L A, van de Putte L B, Zwarts W A

出版信息

Am J Pathol. 1987 Apr;127(1):15-26.

Abstract

Chronicity of murine allergic arthritis depends on the charge-mediated retention of the cationic antigen in the joint. The authors examined whether arthritis induced with the positively charged antigen amidated bovine serum albumin (aBSA) could be modulated with a nonimmunogenic polycation by competition for anionic retention sites in the joint. Concomitant intraarticular injection of aBSA with the cationic protein protamine chloride (pI approximately 10) strongly reduced the retention of aBSA. Detailed analysis revealed that the retention of aBSA in the noncartilaginous tissues was significantly reduced by protamine, whereas the retention in the highly negatively charged cartilage was completely prevented. Joint inflammation was already significantly suppressed at Day 3 and suppression was still demonstrable at Day 28. Protamine treatment also caused a highly significant reduction in cartilage damage and bone apposition. Control experiments indicated that the suppressive effect of protamine was related to its interference with antigen retention in the joint and not to a mere antiinflammatory action.

摘要

小鼠过敏性关节炎的慢性化取决于阳离子抗原在关节中的电荷介导保留。作者研究了用带正电荷的抗原酰胺化牛血清白蛋白(aBSA)诱导的关节炎是否可以通过一种非免疫原性聚阳离子竞争关节中的阴离子保留位点来进行调节。将aBSA与阳离子蛋白氯化鱼精蛋白(pI约为10)同时进行关节内注射,可显著降低aBSA的保留。详细分析表明,鱼精蛋白可显著降低aBSA在非软骨组织中的保留,而在高负电荷的软骨中则完全阻止了aBSA的保留。在第3天关节炎症就已得到显著抑制,并且在第28天仍可观察到抑制作用。鱼精蛋白治疗还导致软骨损伤和骨附着显著减少。对照实验表明,鱼精蛋白的抑制作用与其对关节中抗原保留的干扰有关,而不仅仅是抗炎作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e0a/1899603/8abf20c5af33/amjpathol00145-0025-a.jpg

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