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目的 建立自身免疫性强直性脊柱炎(AS)实验动物模型 ,并探讨重组人蛋白聚糖Versican的G1区多肽 (VG1 )在其脊柱和骶髂关节炎发病中的作用。方法 用自然折叠的VG1和完全弗氏佐剂免疫BALB/c小鼠 ,诱导产生脊柱炎和骶髂关节炎 ,建立自身免疫性AS实验动物模型。采用组织病理学方法显示脊柱炎小鼠的发病程度和病理学特征。结果 用VG1和完全弗氏佐剂免疫的实验组小鼠脊柱炎和骶髂关节炎的发病率分别为 35 0 %和 1 2 5 % ,未出现外周炎的临床症状。组织病理学结果显示 ,脊柱韧带与椎间盘连接处、椎间盘和骶髂关节有大量的单个核细胞浸润。结论 成功建立了VG1诱导的小鼠脊柱炎模型 ,并发现针对蛋白聚糖Versican的免疫反应参与了BALB/c小鼠脊柱炎和骶髂关节炎的发病 ,为进一步深入研究人类AS的发病机制及其临床治疗提供了有价值的实验材料
OBJECTIVE: To establish an animal model of autoimmune ankylosing spondylitis (AS) and to explore the role of recombinant human proteasome G1 glycoprotein (VG1) in the pathogenesis of spondylolisthesis and sacroiliitis. Methods BALB / c mice were immunized with natural folded VG1 and complete Freund’s adjuvant to induce spondylitis and sacroiliitis, and to establish an animal model of autoimmune AS. Histopathological methods were used to show the pathogenesis and pathological features of spondylitis in mice. Results The incidences of spondylitis and sacroiliitis in mice immunized with VG1 and complete Freund’s adjuvant were 35 0% and 125%, respectively. There were no clinical symptoms of peripheral inflammation. Histopathological findings showed extensive mononuclear cell infiltration of the ligaments and intervertebral discs, intervertebral discs and sacroiliac joints. Conclusions VG1-induced mouse spondylitis model was successfully established and it was found that immune response against Versican of proteoglycans was involved in the pathogenesis of spondylitis and sacroiliitis in BALB / c mice. In order to further study the pathogenesis of human AS, Its clinical treatment provides valuable experimental materials