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

Figure 1

Increased p-PKCδ and p-p66Shc expression and ROS production in renal tissues of patients with diabetic nephropathy (DN). Renal biopsy samples were collected from 16 of DN patients and 16 of non-DN patients. Tubular atrophy and interstitial fibrosis were seen in renal biopsies in patients with DN as detected by PASM and PAS staining (panels (B) and (D) versus panels (A) and (C)). Immunohistochemical studies revealed increased expression of p-PKCδ and p-p66Shc in DN patients (panels (F) and (H) versus panels (E) and (G)) (magnification ×200). Status of oxidant stress in kidneys of DN and non-DN patients indicated in panels (I) and (J). ((b) and (c)) Averaged relative intensity following staining of anti-p-PKCδ and anti-p-p66Shc antibody of renal biopsies of DN patients versus non-DN patients. (d) Relative fluorescence intensity of dihydroethidium (DHE) in kidneys of DN and non-DN patients. (e) Tubular interstitial damage score in DN patients versus non-DN patients. (f) Table shows correlation between p-PKC and p-p66Shc expression, DHE level, and tubular interstitial damage. Values are means ± SEM, .