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Cytoprotection by pro-vitamin C against ischemic injuries in perfused rat heart together with differential activation of MAP kinase family

✍ Scribed by Masahiro Eguchi; Mayumi Fujiwara; Yoichi Mizukami; Nobuhiko Miwa


Publisher
John Wiley and Sons
Year
2003
Tongue
English
Weight
149 KB
Volume
89
Category
Article
ISSN
0730-2312

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✦ Synopsis


Abstract

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.


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## Abstract The reactive oxygen species (ROS) are known to be generated upon post‐ischemic reperfusion (I/R) of the heart, and to injure cardiac muscle cells. The hydrogen peroxide‐induced mortality of rat cardiomyoblasts H2c9 was markedly inhibited by previous administration with auto‐oxidation‐re