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. 2017 May 19;8(28):46286–46297. doi: 10.18632/oncotarget.18000

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Copyright: © 2017 Chen et al.

This article is distributed under the terms of the Creative Commons Attribution License (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited.

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(A, B) Bisulfite sequencing shows the methylation of RASgrf1 promoter segment 1 (31 CpG sites) in control mice (control group), KA-treated mice (SE group) and RG108-pretreated mice (RG group) at different time points. There was an increase in the methylation of RASgrf1 after the onset of epileptic seizures, *P < 0.05, compared with the control group. RG108 pretreatment inhibited the increase in the methylation of segment 1, as shown 10 days after the onset of epileptic seizures, ^#P < 0.05. (C, D) Bisulfite sequencing shows the methylation of RASgrf1 promoter segment 2 (26 CpG sites) in control mice (control group), KA-treated mice (SE group) and RG108-pretreated mice (RG group) at different time points. Compared with the control group, RASgrf1 methylation did not show a regular change at segment 2, nor did RG108 significantly affect segment 2 after the onset of epileptic seizures. Filled circles represent methylated CpG sites, and open circles represent unmethylated CpG sites (each group n = 4).