中文摘要：

目的深入揭示氢醌（HQ）致MPL转录激活的表观遗传学机制。方法以磷酸盐缓冲液（PBS）溶解HQ，以正常TK6细胞、PBS处理细胞为对照组，分别以2．5、5．0、10．0和20．0μmol／LHQ染毒TK6细胞为染毒组。应用实时荧光定量一聚合酶链反应检测甲基化CpG结合蛋白1～5（MBD1～5）的表达。结果与对照细胞相比，MBD1—4的mRNA表达量在所有的HQ处理细胞中全部下降，20．0μmol／LHQ对MBD2和MBD4表达的抑制效果最为明显，抑制率分别为50％和32％（P〈O．05）；而10．0μmo1／LHQ对MBD1和MBD3表达的抑制效果最明显，抑制率分别为36％和33％（P〈0．05）；MBD5表达无统计学意义（P〉0．05）。在MPL的CpG岛内有3个MBD1序列特异性结合位点。结论HQ致MPL的转录激活可能与MBD1表达异常有关。

英文摘要：

Objective To explore the epigenetie mechanism of MPL transcriptional activation induced by hydroquinone （HQ）. Methods HQ was dissolved with PBS buffer, 2.5, 5.0, 10.0 and 20.0μmol/L hydroquinone were given to TK6 cells, respectively, and the normal TK6 cells and cells treated with PBS were used as controls. Expressions of methyl-CpG-binding domain proteins 1-5 （MBD1-5） were tested by reverse transcription real-time RT-PCR assay. Results The expressions of MBD1-4 in the HQ-treated cells were decreased compared with those of the control cells and the expressions of MBD2 and MBD4 were severely inhibited by 20.0 μmol/L HQ , decreased by 50% and 32% （P〈0.05）, respectively, while the expressions of MBD1 and MBD3 were severely inhibited by 10.0 p, mol/L HQ, decreased by 36% and 33%（P〈0.05）. In CpG island of MPL, there were three sequence-specific biding sites for MBD1. Conclusion Transcriptional activation of MPL induced by HQ may be associated with the dysregulated expression of MBD1.