Figure 5.

FBXL10 attenuated diabetes‐induced oxidative injury and inflammation in vivo. (A) The expression of p67phox in diabetic rat hearts was analyzed by Western blotting and normalized to β‐actin. Data represent the mean ± SD of three independent experiments. *P < 0.05. (B) The mRNA level of P67phox and Gp91phox in diabetic hearts was analyzed by Real‐time PCR. Data represent the mean ± SD of three independent experiments. *P < 0.05. (C) NADPH oxidase activity in diabetic hearts by FBXL10 overexpression. Data represent the mean ± SD of three independent experiments. **P < 0.01. (D) Total SOD activity in diabetic hearts after FBXL10 overexpression. Data represent the mean ± SD of three independent experiments. *P < 0.05. (E) Lipid peroxidation in diabetic hearts. Data represent the mean ± SD of three independent experiments. *P < 0.05. (F) mRNA level of myocardial TNF‐α, IL‐1β and IL‐6 in rats with diabetes. Data represent the mean ± SD of three independent experiments. **P < 0.01; *P < 0.05. (G) CD45 expression in the rat heart with diabetes was analyzed by immunohistochemistry. Data represent the mean ± SD of three independent experiments. *P < 0.05. (H) CD68 expression in the rat heart with diabetes was analyzed by immunohistochemistry. Data represent the mean ± SD of three independent experiments. *P < 0.05