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作 者:乌兰[1] 梁文波[1] 柳晓光[1] 王鸿[1] 李维加[1] 王仁军[1]
出 处:《大连大学学报》2001年第2期70-76,共7页Journal of Dalian University
摘 要:目的为进一步探讨细胞因子在类风湿关节炎中的作用.方法50只SD大鼠以完全弗氏佐剂(FCA)形成AA动物模型.随机分为Ⅰ组(2周)、Ⅱ组(3周)、Ⅲ组(4周)、Ⅳ组(8周)以及Ⅴ组(正常对照).分别对各组大鼠血清前炎症细胞因子TNF-α、IL-6以及抑制性细胞因子 IL-4、 IL- 10水平进行测定(ELISA法).同时检查炎症指标血沉(ESR)、关节肿胀度、病理切片,所有结果进行对比并做动态分析.结果AA大鼠Ⅰ-Ⅲ组ESR水平及关节肿胀度与对照组均有显著差异(P<0.01);TNF-α组水平各组均高于正常(P<0.05,P<0.01,P<0.001);IL-6水平Ⅱ组(P<0.05)、Ⅲ组高于正常;IL-4水平Ⅰ组、Ⅱ组低于正常组,Ⅲ组、Ⅳ组高于正常组,但均无显著性意义;与正常组比较,IL-10水平Ⅰ组(P<0.001)、Ⅱ组(P<0.05)、Ⅲ组均低于正常,Ⅳ组高于正常组并有非常显著性意义(P<0.01);细胞因子动态观察结果,TNF-α、IL- 6水平随急性期(第2周)开始而升高,高峰水平随急性期过去(第8周)而下降.而调节性因子IL-4、IL-10高峰时间滞后于炎症因子,并随慢性期延长而升高.结论AA大?Objective To document the role of cytokines in rhrumatoid arthritis. Methods Fifty SD rats were injected Complete Freund's adjuvant to produce adjuvant arthritis (AA). All rats were divided into groups randomly according to different disease phases. Group(G) Ⅰ (week2), GⅡ (week3), GⅢ (week4), GⅣ (week8) and GⅤ (normal control). Different parameters include serum level of proinflammatory cytokine TNF-α and IL-6, inhibit cytokine IL-4 and IL-10, inflammatory makers ESR, joint swelling rate, pathologic exmination were obtained and analyzed dynamically. Results Inflammatory makers including ESR, joint swelling rate were singificantly different between the AA rats and controls (p<0.01); Level of TNF-α in GⅠ-GⅣ were higher than normal controls (P<0.05, p<0.01, P<0.001, aspectively); IL-6 level was high in group GⅡ (P<0.05) and GⅢ than normal; IL-4 level in group GⅠ and GⅡ were lower than normal and higher in GⅢ and GⅣ, but no statistics significance; IL-10 level were lower in GⅠ, (P<0.01) GⅡ (P<0.05), and GⅢ, but high in GⅣ (p<0.01); Dynamic observation showed that TNF-αa and IL- 6 leves went up with acute phase (2W) of AA and down with chronic phase (8W). The levels of IL-4 and IL-10 went up after inflammatory cytokines and the peak of levels was at the chronic phase when the levels of inflammatory cytokine went down. Conclusions In AA rat model, TNF-α, IL-6 were positively correlated with ESR, joint swelling rate and pathological changes while IL-4 and IL-10 were negatively correlated with inflammation.
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