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

Figure 5

(a) Diagram of DNA methylation of the GPX1 gene promoter was plotted. Black dots indicated methylated sites while white dots indicated demethylated sites. Columns indicated the methylation rate of the GPX1 gene promoter in myocytes from control, AGE, AGE + Se, AGEs+Se + AZA, and AGE + AZA groups (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 (, )); (b) columns indicated the GPX activity in myocytes from control, AGE, AGE + Se, AGE + Se + AZA, and AGE + AZA groups. (c) Columns indicated relative expression levels of GPX1 mRNA in myocytes from control, AGEs, AGE + Se, AGE + Se + AZA, and AGE + AZA groups. (d) Immunoblots of GPX1 and GAPDH were demonstrated. Columns indicated relative expression levels of GPX1 in myocytes from control, AGE, AGE + Se, AGE + Se + AZA, and AGE + AZA groups (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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