The cardiac muscle cells are known to be killed by ischemia-reperfusion (I/R) treatment that produce reactive oxygen species (ROS). We analyzed the function of the autooxidation-resistant pro-vitamin C, 2-O-alpha-D-glucosylated derivative (Asc2G) of ascorbic acid (Asc), in protecting against I/R injury of the heart in rat. The serum release of the intracellular enzyme CPK due to I/R injury decreased upon injection with Asc2G. Out of the mitogen-activated protein (MAP) kinase family members, MAP kinase and JNK underwent the down-regulation in contrast to up-regulation of p38 compared with the I/R-treated control in the absence of Asc2G. These data suggest important roles for differential activation of the MAP kinase family in cytoprotection against I/R injury by Asc2G.
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Eguchi et al. (2003) studied this question.
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