期刊文献+

肾病患儿外周血单个核细胞中白细胞介素1β及其受体拮抗剂的基因表达 被引量:1

IL-1beta, IL-1ra mRNA expression of peripheralblood mononuclear cells (PBMC) in idiopathicnephrotic syndrome (INS) detected by biotin-labelledprobe in situ hybridization
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摘要 为进一步了解原发性肾病综合征(INS)的发病与细胞免疫功能紊乱的关系,作者应用生物素标记cDNA探计、链霉亲合素-硷性磷酸酶检测系统行细胞涂片原位杂交,并用真彩色医学图像分析系统对杂交信号行定量分析,检测4例INS患儿及5例正常儿外周血单个核细胞(PBMC)中的白细胞介素1β(IL-1β)及其受体拮抗剂(IL-lra)信使核糖核酸(mRNA)的表达。结果:在患儿PBMC中,II-1β和IL-lramRNA的表达都明显低于正常对照(108±20比106±31及145±11比307±100,P<0.05)。提示INS时,PBMC中IL-1β及其受体拮抗剂基因表达异常。作者认为其原因可能与多个细胞因子间相互调节失常有关,并分析了所用生物素标记探针杂交技术在儿科临床应用中的优越性。 he pathogenesis of INS is related to the disorderof cellular immunity. Using the in situ hybridization ofbiotin-labeled probe and streptavidin-alkaline phos-phatase conjugate detection sytem. we quantitativelyanalysed by ture colour medical image analysis systemthe expression of IL-1beta , IL-1ra mRNA of peripher-al blood mononuclear cells (PBMC ) from 4 cases of id-iopathic nephrotic syndrome. IL-1beta IL-1ra mRNAexprossion of PBMC in INS were significantly lowerthan those of the normal control (107. 63±20. 80 vs195. 56±31. 14; 144. 45±11. 42 vs 370. 38±100. 48,respectively, P<0. 05 ). The expression of IL-1betamRNA was significantly lower than the IL-1ra mRNAexnression of PBMC in INS (107. 63±20. 80 vs 144.45±11. 42 , P<0. 05 ) . There existed dysregulation ofIL-1 beta, IL-1ra mRNA expression in INS. The ad-vantages of biotin-labelled probe in situ hybridizationwere also discussed.
出处 《中华医学杂志》 CSCD 北大核心 1995年第3期152-154,共3页 National Medical Journal of China
关键词 白细胞介素 基因表达 肾病综合征 Nephrosis Interleukin 1Gene expression(Original artical on page 152)
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参考文献3

  • 1宋玉华,中华血液学杂志,1993年,14卷,74页
  • 2姚智,中国免疫学杂志,1992年,8卷,48页
  • 3姜新猷,中华儿科杂志,1981年,19卷,241页

同被引文献24

  • 1王丹,杨霁云,王宝琳.白细胞介素-2对肾小球上皮细胞部分生物学功能的影响[J].肾脏病与透析肾移植杂志,1995,4(6):507-509. 被引量:1
  • 2Chen HS, Wu MS, Yen TS. Soluble interleukin-2 receptor in patients with glomerular diseases [ J ]. Postgrad Med J, 1995,71 (840) :617- 622.
  • 3Cho BS, Yoon SR, Jang JY. Up-regulation of interleukin- 4 and CD23/FcepsilonRII in minimal change nephrotic syndrome [ J ]. Pediatr Nephrol, 1999,13 (3) : 199-204.
  • 4Matsumoto K, Ohi H, Kanmatsuse K. Interleukin-4 cooperates with interleukin-10 to inhibit vascular permeability factor release by peripheral blood mononuclear ceils from patients with minimal-change nephrotic syndrome [ J ]. Am J Nephrol, 1999,19 ( 1 ) :21-27.
  • 5Zachwieja J, Bobkowski W. Dobrowolska-Zachwieja A. Intracellular cytokines of peripheral blood lymphocytes in nephrotic syndrome [ J ]. Pediatr Nephrol,2002,17 ( 9 ) :733-740.
  • 6Laflam PF, Haraguchi S, Garin EH, et al. Cytokine mRNA profile in lipoid nephrosis: evidence for increased IL-8 mRNA stability [ J ]. Nephron ,2002,91 (4) :620- 626.
  • 7Daniel V, Trautmann Y, Konrad M, et al. T-lymphocyte populations, cytokines and other growth factors in serum and urine of children with idiopathic nephrotic syndrome[ J ]. Clin Nephrol, 1997, 47 (5) :289-297.
  • 8Matsumoto K. Interleukin 10 inhibits vascular permeability factor release by peripheral blood mononuclear ceils in patients with lipoid nephrosis[ J ]. Nephron, 1997,75 (2) : 154-159.
  • 9Matsumoto K, Ohi H, Kanmatsuse K. Interleukin 12 upregulates the release of vascular permeability factor by peripheral blood mononuclear cells from patients with lipoid nephrosis[ J ]. Nephron, 1998, 78(4) :403- 409.
  • 10Matsumoto K, Ohi H, Kanmatsuse K. Effects of interleukin-15 on vascular permeability factor release by peripheral blood mononuelear cells in normal subjects and in patients with minimal-change nephrotic syndrome [ J ]. Nephron, 1999,82 ( 1 ) :32-38.

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