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

Figure 4

Cardiomyocyte injury and myocardial TOPK, PTEN, and Akt protein expression and their phosphorylation status assessed after hypoxia-reoxygenation (HR) with or without SPostC in H9c2 cells under normal glucose. LY or HI were applied, respectively, to block Akt and TOPK activation in H9c2 cells. (a) Cell viability assessed by MTT assay. (b) Lactate dehydrogenase (LDH) release. (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. All values are presented as the of three independent experiments each performed in triplicate. , , and compared with the HR group; ^# and ^## compared with the SPostC group.

(a)

(b)

(c)

(d)

(e)

(f)