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

Figure 7

Cardiomyocyte injury, oxidative stress, and myocardial TOPK, PTEN, and Akt protein expression and their phosphorylation status assessed after HR with or without SPostC and LY in H9c2 cells under HG condition infected with adenovirus encoding rat TOPK (Ad-TOPK) or adenovirus vector (Ad-vector). (a) Cell viability was tested via MTT assay. (b) LDH release in the conditioned medium was analyzed by LDH assay. (c) MDA levels in different groups. (d) Representative western blots. Protein expression of TOPK (e, f), PTEN (g, h), and Akt (i) and their phosphorylation status in H9c2 cells detected by western blots. Mean band density was normalized relative to GAPDH. All values are presented as the of three independent experiments each performed in triplicate. , , and compared with the Ad-vector+HG+HR group; ^#, ^##, and compared with the Ad-TOPK+HG+HR group.

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