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. Author manuscript; available in PMC: 2009 Jun 22.
Published in final edited form as: J Mol Cell Cardiol. 2007 Aug 17;43(5):580–592. doi: 10.1016/j.yjmcc.2007.08.003

Figure 6. Effect of PI3K inhibition on HO-1 induced cytoprotection in vitro and in vivo.

Figure 6

A. Caspase 3 activity in lysates from control and HO-1 transfected H9c2 exposed to normoxia or hypoxia/reoxygenation in the presence or absence of PI3K inhibition with LY 294002. Inhibition of PI3K had no effect on caspase activity in normoxic conditions. However, LY 294002 markedly increased caspase activity in both control and HO-1-transfected cells in response to H/R (* vs. control normoxia; ** vs. control H/R; # vs. HO-1 H/R. p<.05. n=3 independent experiments performed in duplicates). B. Representative bi-ventricular sections showing the effect of PI3K inhibition with LY 294002 on anterior wall infarct in mice pre-treated with intramyocardial injection of AAV-LacZ or AAV-HO-1. C. Infarct size in mouse hearts transduced with either AAV-HO-1 or AAV-LacZ followed by administration of LY294002 before the I/R injury (* vs. lacZ; ** vs. HO-1, p < 0.05; n = 4-5 mice/group)