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作 者:王俭勤[1] 李幼姬[1] 李志坚[1] 张涤华[1] 周道远[1] 许韩师[1] 叶任高[1]
机构地区:[1]中山医科大学附属第一医院肾内科,广东广州510080
出 处:《中山医科大学学报》2001年第3期195-198,共4页Academic Journal of Sun Yat-sen University of Medical Sciences
基 金:中山医科大学 2 11工程资助课题 ( 15 )
摘 要:【目的】了解磷脂酰肌醇三激酶 (PI3 K)在活动性狼疮肾炎患者外周血单个核细胞中的表达 ,并探讨其与Th2细胞因子的关系。【方法】利用免疫沉淀、免疫印迹和RT PCR技术检测 12例正常人和 14例活动性狼疮肾炎患者外周血单个核细胞PI3 K磷酸化产物、IL 6mRNA和IL 10mRNA表达 ,观察PI3 K特异性抑制剂PY2 940 0 2对活动性狼疮肾炎患者外周血单个核细胞IL 6mRNA和IL 10mRNA表达的影响。【结果】自发培养时活动性狼疮肾炎组外周血单个核细胞PI3 K磷酸化产物明显高于健康对照 (1 14± 0 2 3vs0 46± 0 12 ,P =0 0 2 3) ,CD3单抗诱导下活动性狼疮肾炎组PI3 K磷酸化产物表达仍然高于健康对照组 (2 0 9± 0 6 3vs0 6 5± 0 14,P =0 0 16 )。活动性狼疮肾炎组外周血单个核细胞PI3 K磷酸化产物表达量与IL 6mRNA和IL 10mRNA呈正相关关系 (r =0 6 5 2 ,P =0 0 0 8;r =0 718,P =0 0 0 7)。PI3 K特异性抑制剂PY2 940 0 2明显抑制了抗CD3单抗诱导的活动性狼疮肾炎组IL 6mRNA(2 32± 0 5 1vs0 5 7± 0 15 ,P =0 0 0 9)和IL 10mRNA(1 71± 0 33vs0 6 7± 0 11,P =0 0 0 6 )的表达。【结论】PI3 K过度活化可能介导了IL 6和ILTo observe the expression of PI3 K phosphorylated products and elucidate the correlation between PI3 K phosphorylated products and Th2 cytokine in peripheral blood mononuclear cell (PBMC). 14 patients with active lupus nephritis and 12 controls were selected, PI3 K phosphorylated products were detected by immunoprecipitation and Western blotting,RT PCR was used to observe interleukin 6 mRNA and interleukin 10 mRNA expression. In either spontaneous condition or stimulated by anti CD3 antibody, the expression of PI3 K phosphorylated products in patients with active lupus nephritis were higher than those of the controls(1 14±0 23 vs 0 46±(0 12,P=0 023; 2 09±0 63 vs 0 65±0 14,P=0 016). The expression of PI3 K phosphorylated products in active lupus nephritis showed a positive correlation with interleukin 6 mRNA and interleukin 10 mRNA (r=0 652, P=0 008; r=0 718, P=0 007). PY294002,one of specific inhibitor of PI3 K,inhibited significantly the expression of interleukin 6 mRNA(2 32±0 51 vs 0 57±0 15, P=0 009) and interleukin 10 mRNA (1 71±0 33 vs 0 67±0 11, P=0 006) in stimulated PBMC in active lupus nephritis. [Conclusion] PI3 K can involve in the pathogenesis of lupus nephritis by inducing the overexpression of interleukin 6 and interleukin 10.
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