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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/L HQ染毒TK6细胞为染毒组。应用实时荧光定量-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/L HQ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<0.05);而10.0μmol/L HQ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。
Objective To reveal the epigenetic mechanism of hydroquinone (HQ) -induced MPL transcriptional activation. Methods HQ was dissolved in phosphate buffered saline (PBS) and treated with normal TK6 cells and PBS. The cells were treated with 2.5, 5.0, 10.0 and 20.0 μmol / L HQ, respectively. The expression of methylated CpG binding protein 1 ~ 5 (MBD1 ~ 5) was detected by real-time fluorescence quantitative polymerase chain reaction. Results Compared with the control cells, MBD1-4 mRNA expression decreased in all the HQ-treated cells. The inhibitory effect of 20.0μmol / L HQ on the expression of MBD2 and MBD4 was the most obvious with the inhibition rates of 50% and 32%, respectively P <0.05). However, the inhibitory effect of 10.0μmol / L HQ on the expression of MBD1 and MBD3 was the most obvious with the inhibition rates of 36% and 33%, respectively (P <0.05). The expression of MBD5 was not statistically significant (P> 0.05). There are 3 MBD1 sequence-specific binding sites in the CpG island of MPL. Conclusion The transcriptional activation of MPL induced by HQ may be related to the abnormal expression of MBD1.