摘要
目的:研究糖皮质激素诱发的亮氨酸拉链蛋白(GILZ)在特发性血小板减少性紫癜发病机制中的作用。方法:收集已确诊的特发性血小板减少性紫癜(ITP)患者抗凝血26例,利用密度梯度离心法获取外周血单个核细胞(PBMCs),并将PBMCs分为地塞米松(DEX)干预组及空白对照组,相同条件培养48h。采用逆转录-酶联聚合反应(RT-PCR)法检测各组PBMCs中GILZ mRNA及Bcl-2mRNA的表达;酶联免疫吸附法(ELISA)检测Bcl-2蛋白表达量。结果:在10-7 mol/L DEX刺激下,DEX刺激组ITP患者PBMCs的GILZ mRNA表达水平高于空白对照组(P<0.05);DEX刺激组Bcl-2mRNA及Bcl-2蛋白的表达量低于空白对照组(P<0.05)。结论:糖皮质激素可有效上调GILZ基因表达;GILZ的高表达可以下调Bcl-2表达量,具有促进凋亡的作用。
Objective： To investigate the mechanism of the action of glucocorticoid induced leucine zipper（GILZ） in idiopathic thrombocytopenic purpura.Methods： The peripheral blood mononuclear cells（PBMCs） were segregated from twenty six idiopathic thrombocytopenic purpura patients.In one group the cells were treated with dexamethasone（DEX）,while in another group the cells were treated with PBS.Forty eight hours later total RNA were abstracted in both two groups.Reverse transcription polymerase chain reaction（RT-PCR） was used to analysis the expression of GILZ mRNA and Bcl-2 mRNA in PBMCs from both groups.Enzyme linked immunosorbent assay（ELISA） was used to analysis the expression of Bcl-2 protein.Results： The medium GILZ mRNA was increased in idiopathic thrombocytopenic purpura patients at DEX group when compared with controls（P0.05）.Levels of Bcl-2 mRNA and Bcl-2 protein expression decreased in DEX group（P0.05）.Conclusion： DEX is an effective stimulator of GILZ production.Overexpression of GILZ can decrease Bcl-2 concentration in idiopathic thrombocytopenic purpura patients,suggesting that GILZ may have therapeutic value for immunity diseases,such as idiopathic thrombocytopenic purpura.
出处
《武汉大学学报（医学版）》
CAS
北大核心
2012年第2期272-274,279,共4页
Medical Journal of Wuhan University
