Protective Effects of Grape Seed Proanthocyanidin Extract IH636 against Ischemia and Reperfusion Injury in HL-1 Cardiomyocytes

Abstract

One of the major contributors to myocardial cell injury is the increase in ROS as a result of ischemia/reperfusion (I/R) (Vanden Hoek et a/., 1996, 1997). Ischemia refers to a lack of oxygen and metabolic substrates (i.e. glucose) and reperfusion entails re-introducing oxygen and substrates to the cells after ischemia, a progression of conditions which, for example, is experienced by cardiomyocytes during heart surgery. During these two processes, direct damage is incurred by the explosion of oxygen-derived free radicals while indirect myocardial cell damage occurs due to an inflammatory cascade and the synthesis of prostaglandins (Figure 1). Sato et at. (2001) has shown that grape seed proanthocyanidin extract (GSPE) has a strong /n vivo free radical scavenging ability and suggested the protective ability of GSPE to reduce apoptosis by attenuating I/R-induced proliferation of proapoptotic transcription factor JNK-1. Hence while it is known that GSPE has free radical scavenging ability, a short-term effect, it is also important to investigate the possibility that ROS protection could result from long-term treatments that affect protein synthesis. By studying the effect of acute vs. chronic GSPE treatment on apoptosis and necrosis of HL-1 cardiomyocytes subjected to I/R conditions, the mechanism by which GSPE shields cardiomyocytes from electrophilic and ROS injury will be further elucidated.