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Cytoprotection by pro‐vitamin C against ischemic injuries in perfused rat heart together with differential activation of MAP kinase family
Author(s) -
Eguchi Masahiro,
Fujiwara Mayumi,
Mizukami Yoichi,
Miwa Nobuhiko
Publication year - 2003
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.10577
Subject(s) - cytoprotection , ascorbic acid , p38 mitogen activated protein kinases , kinase , mitogen activated protein kinase , protein kinase a , intracellular , reperfusion injury , chemistry , ischemia , reactive oxygen species , cardiac function curve , pharmacology , medicine , endocrinology , biochemistry , oxidative stress , heart failure , food science
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. J. Cell. Biochem. 89: 863–867, 2003. © 2003 Wiley‐Liss, Inc.