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

Figure 4

Rottlerin inhibits HG-induced p66Shc phosphorylation in HK-2 cells. Cells were treated with Rottlerin for 30 min prior to HG (30 mM) treatment. Total proteins were collected for Western blot analysis of p-p66Shc, total p66Shc, and β-actin ((a) and (b)). (c) By immunocytofluorescence microscopy, the increased phosphorylation of PKCδ and p66Shc was seen in HK-2 cells after treatment with 30 mM HG, while this effect was significantly attenuated in Rottlerin group. Values are means ± SEM, . versus LG group, versus HG-only group.

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(b)

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