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作 者:张凯[1] 黄津[1] 赵文君[2] 邢国胜[2] 陆金红[1] 王毅[1] 魏学磊[2] 于顺禄[2] 陆芸[2]
机构地区:[1]天津市天津医院检验科,天津300211 [2]天津市天津医院骨研所,天津300211
出 处:《中国免疫学杂志》2011年第11期1015-1017,共3页Chinese Journal of Immunology
基 金:天津市科委面上项目(07JCYBJ10500)资助
摘 要:目的:通过分析比较类风湿关节炎(Rheumatoid Arthritis,RA)患者血清和外周血单个核细胞(Peripheral bloodmononuclear cell,PBMC)IL-23的表达,探讨其在RA发病过程中的作用,以期为治疗开辟新途径。方法:应用ELISA方法检测RA、骨性关节炎(Osteoarthritis,OA)及正常对照组血清中IL-23和TNFα-蛋白水平,采用RT-PCR法测定各组PBMC中IL-23p19mRNA的表达,并作血清IL-23含量、PBMC IL-23p19mRNA的表达与血清TNFα-水平的相关分析。结果:RA组血清IL-23水平高于正常对照组(P=0.001),其他组间无统计学差异(分别为P=0.122,P=0.127);而各组血清TNFα-的水平均具有统计学差异,RA和OA组均高于对照组(P=0.000,P=0.042),RA组也高于OA组(P=0.013);RA组IL-23p19mRNA的表达高于OA和正常对照组(P=0.000,P=0.000),而OA组与正常对照组差异无统计学意义(P=0.628);血清中IL-23和TNFα-的相关性无统计学差异(r=0.212,P=0.262),而PBMC中IL-23p19mRNA的表达与血清TNFα-呈正相关关系(r=0.392,P=0.032)。结论:IL-23在RA患者PBMC中高表达,在RA的炎性发展过程起到了重要作用。Objective:To determine the level of IL-23 in peripheral blood mononuclear cell(PBMC) and serum in patient with rheumatoid arthritis(RA),and analyze its role in the pathogenesis.Methods:The level of IL-23 and TNF-α in serum of RA,OA and control groups were detected by immunohistochemistry.The expression of IL-23p19mRNA in human PBMC was measured real-time PCR.Results:The level of IL-23 in RA serum was higher than control(P=0.001),and was not significantly different from other groups(P=0.122,P=0.127).Both the level of TNF-α in serum of RA and OA patients were significantly higher than that of the control(P=0.000,P=0.042),TNF-α in serum from RA patients was also higher than that of OA(P=0.013).Expression of the IL-23p19mRNA in PBMC from RA was significantly higher than that of OA and control(P=0.000,P=0.000),there is no significantly different between OA and control(P=0.628).No significant relationship between level of the IL-23 and that of TNF-α in serum of RA(r=0.212,P=0.262),while expression of the IL-23p19mRNA in PBMC from RA patients was significantly associated with level of TNF-α in serum(r=0.392,P=0.032).Conclusion:The level of IL-23 was significantly high in PBMC of RA patients,may be important in the pathogenesis of RA.
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