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作 者:路跃武[1] 陈文明[2] 陆江阳[3] 董馨[1] 郑毅[1]
机构地区:[1]首都医科大学附属北京朝阳医院风湿免疫科,北京100020 [2]首都医科大学附属北京朝阳医院血液科,北京100020 [3]中国人民解放军第三○四医院病理科
出 处:《天津医药》2007年第3期170-172,共3页Tianjin Medical Journal
摘 要:目的:检测类风湿关节炎(RA)患者血清瘦素水平、滑膜中瘦素及瘦素受体的表达,探讨瘦素在RA发病中的作用机制。方法:RA患者血清标本30例(RA组),以酶联免疫吸附试验(ELISA)测定其血清瘦素浓度;关节滑膜标本25例,用免疫组化的方法测定瘦素及瘦素受体在滑膜中的表达;并与25例骨性关节炎(OA)组和3例正常者(对照组)比较。结果:RA组患者血清瘦素水平明显高于骨性关节炎(OA)组(P<0.01),也明显高于滑液水平(P<0.05);且与体质量指数、a1酸性糖蛋白呈正相关(标准化回归系数分别为0.369及0.234;P<0.01);与握力、胰岛素指数及空腹血糖呈负相关(标准化回归系数分别为-0.295、-0.453及-0.192;P<0.01)C与胰岛素水平、C反应蛋白、类风湿因子(RF)、肿胀指数、压痛指数、晨僵时间、病程、年龄、性别等无关;瘦素及瘦素受体在RA患者滑膜中的表达明显高于正常对照组。结论:瘦素可能通过在靶器官的高表达而起到调节炎症的作用;可能在炎性反应中参与急性时相蛋白的合成与调节而影响疾病的发展过程。Objective: To determine the level of serum leptin and the expressions of leptin and leptin receptor on synovial membranes in rheumatoid arthritis (RA), and explore the pathogenesis of leptin in RA. Methods: Leptin levels in the serum of 30 RA patients were measured by enzyme-linked immunosorbent assay (ELISA), and the expressions of leptin and leptin re- ceptor on synovial membranes in 25 RA patients were investigated by immunohistochemical. The results were compared with those in 25 osteoarthritis patients and 3 normal controls. Results: Leptin levels in RA patients were significantly higher than those in osteoarthritis patients(P 〈 0.01) and higher than those in synovial fluid (P 〈 0.05). Leptin level was positively correlat- ed to body mass index (BMI) and ctl acid glycoprotein (AAG), standard regression index were 0.369 and 0.234 (P 〈 0.01) and it was negatively correlated to power grasp, insulin index and blood glucose, standard regression index were -0.295, -0.453 and -0.192(P 〈 0.01). There was no significant difference between leptin and insulin level, C-reaction protein (CRP), rheumatoid factor (RF), swelling index, tenderness index, morning stiffness time, course of diseases, ages and sex. Leptin and leptin receptor expressions of synovial membranes in RA patients were higher than those in controls. Conclusiort Leptin may affect inflammatory by high expression on target organs and influence disease development by modulating the synthesis of acute phase protein.
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