[Retracted] PKCδ Promotes High Glucose Induced Renal Tubular Oxidative Damage via Regulating Activation and Translocation of p66Shc

Figure 2

HG induced phosphorylation of PKCδ and p66Shc in HK-2 cells in a dose-dependent manner. Protein expression of PKCδ and p66Shc and their phosphorylation in HK-2 cells following exposure to HG (5–45 mM) for 120 min were determined by Western blot analysis. 45 mM of D-mannitol as an osmotic control. Phosphorylation of both PKCδ and p66Shc increased in a dose-dependent manner in HK-2 cells treated with high glucose. No change was observed in the expression of total protein of PKCδ and p66Shc; β-actin served as a loading control (a). ((b) and (c)) The bar graphs represent the expression of p-PKCδ and p-p66Shc relative to PKCδ and p66Shc, respectively. Values are means ± SEM; . , versus control.

(a)

(b)

(c)