摘要
目的探讨滑液中肿瘤坏死因子(tumor necrosis factor- a, TNF- a)生物活性及滑膜细胞分泌TNF-α能力的变化在骨关节炎(osteoarthritis,OA)致病机制中的作用。方法应用TNF-a对L929细胞杀伤作用的比色法,检测并比较分析OA与不同年龄、不同形式关节内创伤时滑液和血清中TNF-α生物活性,以及培养的OA、急性关节内创伤和正常滑膜细胞自分泌及诱生性TNF-α生物活性的变化。结果OA的滑液和血清中、老年慢性关节内创伤血清中、急性关节内创伤滑液中含较高水平的TNF-α。培养的 OA和急性关节内创伤滑膜细胞可自分泌TNF-α,对细菌脂多糖(lipopolysaccharide,LPS)刺激的反应性和敏感性较正常滑膜细胞增强,分泌TNF-a的能力提高,诱生性TNF-a的量与LPS呈时间一效应和剂量一效应的依赖关系。结论OA滑液中高水平的TNF—a与其血清中异常升高的TNF-a和滑膜细胞变性有关,而急性关节内创伤的滑液中高水平的TNF-a可来源于变性的滑膜细胞。滑液中TNF—a的异常升高和滑膜细胞变性,是OA发生、发展的重要介导因素。
Objective TO investigate the changes of biological features of synoviocytes in synthesizing and secreting tumor necrosis factor -- a (TNF -- a) in the pathogenesis of osteoarthritis(OA). Methods Synovial fluid(SF) and serum were collected from patients with OA and from patients with chronic and acute joint trauma and normal joints. The synoviocytes were isolated from these specimens alld cultured. The bioactivity of TNF -- a in SF, serum and that produced by the synoviocytes were detected with method of L 929 cells killing test. Results The bioactivity of TNF -- ac both in SF and serum were higher in patients with OA, and the bioactivity of TNF -- a were higher in serum in patients with chronic traumatic joint or in SF in patients with acute traumatic joint. The level of TNF -- a spontaneously produced by the synoviocytes in OA and in acute traumatic joint and the sensibility of these cells to LPS -- induced TNF -- a secretion were also higher. LPS in doses from I ig/Inl to 10 ig/ml and in phase from 4 to 48 hours stimulated dose-dependent and time-dependent increase of TNF -- a. Conclusion TNF -- a may originate from serum in aged people or from synoviocytes with abnormal function and is associated with destructive process in OA.
出处
《中华骨科杂志》
CAS
CSCD
北大核心
1999年第12期726-729,共4页
Chinese Journal of Orthopaedics
关键词
肿瘤坏死因子
骨关节炎
滑液
滑膜
Tumor necrosis factor Osteoarthritis Synovial fluid Synovial membrane28- 34岁,平均( 3121. 2)岁,作为年轻急性关节内