INT-767 treatment prevents the increase in renal inflammation and oxidative stress in diabetic DBA/2J mice. INT-767 treatment prevents the increase in.

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INT-767 treatment prevents the increase in renal inflammation and oxidative stress in diabetic DBA/2J mice. INT-767 treatment prevents the increase in renal inflammation and oxidative stress in diabetic DBA/2J mice. (A) Immunofluorescence staining of kidney sections for CD68 (red) and wheat germ agglutinin (staining whole nephron; green) indicates increased CD68 staining in the diabetic kidney, which is prevented by INT-767. (B) p65 and p50 mRNA abundance is increased in the diabetic kidney, which is prevented by INT-767. (C) Renal NF-κB transcriptional activation determined by DNA binding assay is increased in the diabetic kidney, which is prevented by INT-767. (D) Oxidative carbonylation of proteins in kidney homogenate as measured by ELISA is increased in the diabetic kidney, which is prevented by INT-767. (E) Nox-2 and p22-phox mRNA are increased in the diabetic kidney, which is prevented by INT-767. Nox-4 gene is not regulated. CON, nondiabetic DBA/2J. *P<0.05 versus CON (n=6 mice per group); †P<0.05 versus STZ (n=6 mice per group). Xiaoxin X. Wang et al. JASN 2018;29:118-137 ©2018 by American Society of Nephrology