Selenium Supplementation Improved Cardiac Functions by Suppressing DNMT2-Mediated GPX1 Promoter DNA Methylation in AGE-Induced Heart Failure

Figure 4

(a) Columns indicated relative mRNA expression levels of DNMT1, DNMT2, DNMT3a, and DNMT3b in cardiac tissue of rats from control, AGE, and AGE + Se groups. (b) Immunoblots of DNMT1, DNMT2, DNMT3a, and DNMT3b. Columns indicated relative expression levels of DNMT1, DNMT2, DNMT3a, and DNMT3b in cardiac tissue of rats from control, AGE, and AGE + Se groups (control: rats treated with control BSA; AGEs: rats treated with AGE-BSA; AGEs + Se: rats treated with AGE-BSA then supplemented with sodium selenite ( or 10, )). (c) Columns indicated relative mRNA expression levels of DNMT1, DNMT2, DNMT3a, and DNMT3b in myocytes from control, AGEs, AGE + Se, AGE + Se + AZA, and AGE + AZA groups, respectively. (d) Immunoblots of DNMT1, DNMT2, DNMT3a, and DNMT3b. Columns indicated relative expression levels of DNMT1, DNMT2, DNMT3a, and DNMT3b in myocytes from control, AGEs, AGE + Se, AGE + Se + AZA, and AGE + AZA groups, respectively (control: myocytes treated with control BSA; AGEs: myocytes incubated with AGEs; AGEs + Se: AGE-exposed myocytes treated with sodium selenite; AGEs + Se + AZA: AGE-exposed myocytes treated with sodium selenite and AZA; AGEs + AZA: AGE-exposed myocytes treated with AZA ( or 10, )).

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