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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。
AIM: To investigate the role of glucocorticoid-induced leucine zipper protein (GILZ) in the pathogenesis of idiopathic thrombocytopenic purpura. Methods: Twenty-six patients with idiopathic thrombocytopenic purpura (ITP) were enrolled in this study. Peripheral blood mononuclear cells (PBMCs) were obtained by density gradient centrifugation. PBMCs were divided into three groups: dexamethasone (DEX) Group and blank control group, under the same conditions for 48h. The expression of GILZ mRNA and Bcl-2 mRNA in PBMCs of each group was detected by reverse transcription-polymerase chain reaction (RT-PCR), and the protein expression of Bcl-2 was detected by enzyme linked immunosorbent assay (ELISA). Results: The expression of GILZ mRNA in PBMCs of ITP patients treated with 10-7 mol / L DEX was higher than that of blank control group (P <0.05). The expression of Bcl-2 mRNA and Bcl-2 protein in DEX stimulation group was lower In the blank control group (P <0.05). CONCLUSION: Glucocorticoid can effectively up-regulate the expression of GILZ gene. High expression of GILZ can down-regulate the expression of Bcl-2 and promote apoptosis.