Inhibition of HDAC6 Activity Alleviates Myocardial Ischemia/Reperfusion Injury in Diabetic Rats: Potential Role of Peroxiredoxin 1 Acetylation and Redox Regulation

Figure 8

Effects of TubA on ROS, mPTP, apoptosis rate, and cellular injury in Prdx1-WT-HA- and Prdx1-K197R-HA-transfected H9c2 cells exposed to HG. HG: high glucose (30 mM); HR: hypoxia/reoxygenation; TubA: tubastatin A; WT: Prdx1-WT-HA-transfected H9c2 cells; K197R: Prdx1-K197R-HA-transfected H9c2 cells. (a) Representative immunoblot showing expression of Acetyl-K and HA in Prx1-WT- or Prdx1-K197R-transfected H9C2 cells. GAPDH served as the loading control. (b) Cardiomyocyte cell viability. (c) Cardiomyocyte LDH release. (d) Cardiomyocyte superoxide anion production. (e) Cardiomyocyte superoxide anion production. (f) Representative images of ROS staining and the mean fluorescence intensity of DCFDA in each group. (g) Representative images of flow cytometry and cardiomyocyte apoptosis rates in each group. (h) Fluorescent images of the cells show the change in integrity of mPTP. All values are presented as the mean ± SEM, /group. versus WT-HG group, versus WT-HGHR group, versus K197R-HG group, and versus WT-HGHR + TubA group.