Oxidative Medicine and Cellular Longevity / 2019 / Article / Fig 10

Research Article

Hyperglycemia-Induced Oxidative Stress Abrogates Remifentanil Preconditioning-Mediated Cardioprotection in Diabetic Rats by Impairing Caveolin-3-Modulated PI3K/Akt and JAK2/STAT3 Signaling

Figure 10

N-Acetylcysteine- (NAC-) preserved remifentanil protection against HG and H/R-induced injury requires intact Cav-3-modulated PI3K/Akt and JAK2/STAT3 signaling in H9C2 cells. H9C2 cells transfected with or without Cav-3 siRNA, Akt siRNA, or STAT3 siRNA were treated with or without remifentanil (Remi, 2.5 μM) treatment in the presence of NAC (1 mmol/L) and high glucose (HG) with normoxia (Nor) for 36 h, then subjected to 4 hours of hypoxia followed by 4 hours of reoxygenation (H/R). LDH release (a), O2- production (b), percentage of JC-1 monomeric cells in total cells (c), and Cav-3 (d), Akt (e), and STAT3 (f) expression and their phosphorylation. All the results are expressed as , . Differences were determined by one-way analysis of variance (ANOVA) followed by Tukey’s test. vs. the HG+NAC+H/R group; vs. the HG+NAC+H/R+Remi group.