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. Author manuscript; available in PMC: 2010 Jul 22.
Published in final edited form as: Alcohol Clin Exp Res. 2008 Nov 19;33(2):206–219. doi: 10.1111/j.1530-0277.2008.00828.x

Figure 3. Protein kinase Cε is a key factor in alcohol-mediated cardioprotection.

Figure 3

Submitochondrial particles were prepared as described (Zhou et al., 2004) from hearts of alcohol-fed (black bars) and control (white bars) mice and used to measure respiratory chain complex activities after ischemia-reperfusion. (A) Moderate alcohol intake significantly improved mitochondrial NADH-oxidase activity after stress. In contrast, sustained cardioprotection was blocked by a protein kinase Cε antagonist peptide and in knockout mice. (B) Chronic protection against NADH-Q1 reductase (Complex I) injury was also abolished by protein kinase C inhibition. n = 6 hearts per condition. *P<0.05 vs. control ischemia-reperfusion hearts.