Skip to main content
. 2018 Sep 9;8(17):4664–4678. doi: 10.7150/thno.26619

Figure 7.

Figure 7

ICL1-9 decreases H/R-induced caspase 3/7 activity and superoxide formation in cardiomyocytes via RhoA/ROCK activation. NRVM underwent hypoxia for 4 h followed by reoxygenation for 20 h in the presence of Veh, Scr or ICL1-9 pepducin (10 µM each) with or without pretreatment with ICI 118,551 (100 nM), Y-27632 (10µM) or Rhosin (10 µM). Caspase 3/7 activity (A-B) was assessed as in Figure 5 and superoxide formation (C-D) was measured using mitosox red. Values are expressed as a percentage of H/R Veh (A, C) or Veh Scr (B, D). For (A): n=9 for all treatment groups, for (B): n=12 for all treatment groups, for (C): n=8 Veh and H/R Veh, n=14 H/R Scr and H/R ICL1-9, for (C): n=14 for Veh Scr and Veh ICL1-9, n=8 for all other treatment groups. ns = not significant, * p < 0.05, *** p < 0.001, one-way ANOVA with Tukey's multiple test. (E) Representative images of mitoSOX staining (red) in NRVM with or without H/R (left panels) or H/R plus Veh, ICI 118,551 (100 nM), Y-27632 (10µM) or Rhosin (10 µM) and Scr or ICL1-9 pepducin (10 µM each, right panels). Cells were counterstained with DAPI (blue) to detect nuclei. n=5 for Veh No H/R and Veh H/R, n=6 for Veh H/R Scr and Veh H/R ICL1-9, n=4 for all other H/R treatment groups.