Research Paper Volume 12, Issue 12 pp 11325—11336

CD38 inhibition by apigenin ameliorates mitochondrial oxidative stress through restoration of the intracellular NAD+/NADH ratio and Sirt3 activity in renal tubular cells in diabetic rats


Figure 5. CD38 knockdown increases Sirt3 activity and intracellular NAD+/NADH ratio in renal proximal tubular cells grown in high glucose. (A) Western blots of CD38, Sirt3, ace (Lys413)-IDH2, IDH2, ace (Lys68)-SOD2, and β-actin in HK-2 cells cultured in low and high glucose after transfection using scrambled or CD38 siRNA. (BE) Densitometric evaluation of CD38 to β-actin (B), Sirt3 to β-actin (C), Ace-IDH2 to IDH2 (D), and Ace-SOD2 to SOD2 (E) immunoblotting data shown in panel A (n=4). (F) Intracellular NAD+/NADH ratio in cultured HK-2 cells under the above conditions (n= 4). All data represent the mean ± standard deviation (SD). *p<0.01 vs. the indicated group, **p<0.05 vs. the indicated group, n.s; not significant.