激肽原缺乏对炎性关节炎大鼠模型炎症的调节作用
Modulation of inflammation by kininogen deficiency in a rat model of inflammatory arthritis.
作者信息
Sainz Irma M, Isordia-Salas Irma, Castaneda Julian L, Agelan Alexis, Liu Bo, DeLa Cadena Raul A, Pixley Robin A, Adam Albert, Sartor R Balfour, Colman Robert W
机构信息
Temple University, Philadelphia, PA 19140, USA.
出版信息
Arthritis Rheum. 2005 Aug;52(8):2549-52. doi: 10.1002/art.21202.
OBJECTIVE
To compare inflammatory peripheral arthritis in wild-type and high molecular weight kininogen (HK)-deficient rats, both on the genetically susceptible Lewis background.
METHODS
By backcrossing Brown-Norway HK-deficient rats with Lewis rats for 6 generations, 2 new strains were produced, wild-type F6 and HK-deficient F6, each with a 98.5% Lewis genome. Inflammatory arthritis was induced by intraperitoneal injection of peptidoglycan-polysaccharide (PG-PS), and the clinical, histopathologic, and biochemical responses were compared in both strains.
RESULTS
Eighteen days after PG-PS injection, rats with normal concentrations of HK showed weight loss and marked increase in hind ankle diameter with severe synovial inflammation and cartilage abnormalities. In contrast, HK-deficient rats showed no weight loss (P < 0.05), no increase in hind ankle diameter (P < 0.05), and an absence of inflammatory changes (P < 0.05), as measured by the histologic and morphometric Mankin grading system for synovial and cartilage injury.
CONCLUSION
Plasma HK is a key mediator of acute and chronic inflammatory arthritis in genetically susceptible Lewis rats.
目的
比较在基因易感的Lewis背景下野生型和高分子量激肽原（HK）缺陷型大鼠的炎性外周关节炎。
方法
通过将Brown-Norway HK缺陷型大鼠与Lewis大鼠回交6代，培育出2个新的品系，野生型F6和HK缺陷型F6，每个品系的Lewis基因组含量均为98.5%。通过腹腔注射肽聚糖-多糖（PG-PS）诱导炎性关节炎，并比较两个品系的临床、组织病理学和生化反应。
结果
注射PG-PS 18天后，HK浓度正常的大鼠出现体重减轻，后踝关节直径显著增加，伴有严重的滑膜炎和软骨异常。相比之下，HK缺陷型大鼠未出现体重减轻（P<0.05），后踝关节直径未增加（P<0.05），并且通过用于评估滑膜和软骨损伤的组织学和形态计量学Mankin分级系统测量，未出现炎症变化（P<0.05）。
结论
血浆HK是基因易感的Lewis大鼠急性和慢性炎性关节炎的关键介质。
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