Inactivation of TOPK Caused by Hyperglycemia Blocks Diabetic Heart Sensitivity to Sevoflurane Postconditioning by Impairing the PTEN/PI3K/Akt Signaling

Figure 5

Oxidative stress and myocardial TOPK, PTEN, and Akt protein expression and their phosphorylation status assessed after myocardial IR with or without SPostC in nondiabetic and diabetic mice. (a) Representative photographs of dihydroethidium (DHE) staining detected by immunofluorescence in the mouse hearts. (DAPI: nuclei, blue; DHE fluorescence: red; magnification, ×400). (b) Serum levels of malondialdehyde (MDA) assessed by a kit. (c) Representative western blots. (d–f) Expression of TOPK (d), PTEN (e), and Akt (f) and their phosphorylation status. Mean band density was normalized relative to GAPDH. The IR group was used as control and normalized to unity, and the protein expression of other groups was displayed as changes over this baseline. (g) Myocardial phosphorylated TOPK level detected by immunofluorescence. All values are presented as the ( per group). and compared with the IR group.

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