Cox-2 Inhibition Protects against Hypoxia/Reoxygenation-Induced Cardiomyocyte Apoptosis via Akt-Dependent Enhancement of iNOS Expression

Figure 8

iNOS primarily mediated cardioprotective effects of NS398 in H/R-induced H9C2 cardiomyocytes apoptosis. (a) Representative original Western blots of iNOS, cleaved caspase-3, total caspase-3, and GAPDH in H9C2 cardiomyocytes with or without H/R stimulation in the presence or absence of NS398 or 1400W (iNOS specific inhibitor, 1 μM, 30 min). iNOS and cleaved caspase-3 were normalized to GAPDH and total caspase-3, respectively. (b) The release of LDH, (c) cell viability, and (d) NO content were determined in H9C2 cardiomyocytes with or without H/R stimulation in the presence or absence of NS398 or 1400W and were expressed against those in CTL group. Data are shown as means ± SEM; CTL versus H/R or H/R + NS398 or H/R + NS398 + 1400W, H/R versus H/R + NS398, and H/R + NS398 versus H/R + NS398 + 1400W (nonparametric Mann–Whitney U test in (a) and one-way ANOVA followed by Tukey’s test in (b), (c), and (d)); per group.

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