Figure 1.
Inhibition of CYP4A with HET0016 reduces myocardial oxidative stress induced by advanced glycation end-products (AGEs) in mice. (A) Protein expression of CYP4A, n = 3. (B) Serum AGEs levels, n = 9. (C) Serum lactate dehydrogenase (LDH) levels, n = 9. (D) H2O2 content in the myocardium, n = 9. (E) Myocardial malondialdehyde (MDA) content, n = 9. (F) Protein expression of NOX2, n = 3. (G) Activity of SOD in the myocardium, n = 9. AGEs solution was administered intragastrically to C57BL/6 mice for 60 days, while the specific inhibitor of CYP4A, HET0016, was given from the 47th day via intraperitoneal injection. Con, control. Compared with the Con group, +p < 0.05, ++p < 0.01; compared with the AGEs group, *p < 0.05, **p < 0.01 (one-way ANOVA with Tukey post hoc).