Research Article

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

Figure 2

Myocardial IR injury and myocardial apoptosis after 45 min coronary occlusion followed by 120 min reperfusion with or without SPostC in nondiabetic and diabetic mice. IR and SPostC indicated nondiabetic mice received IR or IR+SPostC, respectively; IR+SPostC+LY and IR+SPostC+HI indicated nondiabetic mice pretreated with LY294002 (LY, a PI3K inhibitor) or HI-TOPK-032 (HI, a TOPK kinase inhibitor), respectively, and then subjected to IR and SPostC. DM+IR and DM+IR+SPostC indicated diabetic mice received IR or IR+SPostC, respectively. (a) Representative images of Evans blue and TTC staining in heart cross sections from each experimental group. Infarct area (INF: white); area at risk (AAR: red and white); perfused area (blue). (b) Comparison of area at risk per left ventricle (area at risk/left ventricle). (c) Comparison of area of infarct size normalized to the area at risk (infarct size/area at risk). (d) Myocardial apoptosis was assessed by the TUNEL assay in the heart sections (DAPI: nuclei, blue; TUNEL: apoptosis nuclei, green; magnification, ×400). (e) Quantification of TUNEL-positive cardiomyocytes (% of total). (f) Plasma CK-MB secretion detected using a commercial ELISA kit. All values are presented as the ( per group). , , and compared with the IR group; # and ## compared with the SPostC group.
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