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作 者:王静[1] 余爽[1] 陈楚[1] 董冰[1] 鲍依稀[1]
机构地区:[1]重庆医科大学附属第二医院检验科,重庆400010
出 处:《中国免疫学杂志》2013年第3期236-239,共4页Chinese Journal of Immunology
基 金:国家自然科学基金(81274144);重庆市科委课题项目(CSCT 2009BB5399);重庆市教委课题项目(KJ110303);重庆市卫生局中医药科技项目(2010-2-147)资助
摘 要:目的:探讨云芝糖肽(PSP)对乳腺癌患者外周血单个核细胞(PBMC)中TLR信号通路MyD88途径的免疫调节机制。方法:体外分离乳腺癌患者(20例)PBMC并将每份细胞分为2组,设为对照组和PSP组,采用实时荧光定量PCR(Q-PCR)检测各组PBMC中TLR信号通路MyD88途径相关基因的表达情况并进行定量分析,同时使用Western blot检测信号末端蛋白的表达情况。结果:PSP能够显著提高TLR信号通路中TLR4、TLR5、TLR6、IRAK4、TRAF6、IRF5、TAK1、IKKα、NF-κB、ERK、P38、JNK、AP-1、IL-1β和IL-8基因的相对表达量(P<0.01),信号末端蛋白NF-κB、AP-1和IRF5均有上调。结论:PSP对乳腺癌患者PBMC中TLR通路的调控可能主要是通过MyD88途径促使终端效应因子的释放从而发挥其免疫调节作用。Objective:To detect the effects of polysaccharopeptide (PSP) on TLR signaling pathway in breast cancer patient's peripheral blood mononuclear cells (PBMCs). Methods: After isolation of PBMC from breast cancer patient, cells were divided into control group and PSP group. Quantitative real-time PCR (Q-PCR) and Western blot were used to detect the related gene and protein expression of TLR pathway regulated by PSP. Results: Genes in TLR/MyD88 pathway were up-regulated significantly by PSP: TLR4, TLRS, TLR6, IRAK4, TRAF6, IRFS, TAK1, IKKct, NF-KB, ERK, P38, JNK, AP-1, IL-113 and IL-8 (P 〈 0. O1 ). Meanwhile, the terminal effect proteins (NF-RB, AP-1 and IRF5 ) were up-regulated significantly by PSP. Conclusion: PSP takes its immunoregu- latory effect on TLR signaling pathway through MyD88 in patients with breast cancer.
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