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The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
Published on: June 17, 2016
Activation of mitogen activated protein kinase (MAPK) during D-galactosamine intoxication in the rat liver
Hitomi Nishioka1, Terumi Kishioka, Chinatsu Iida
1Department of Food Science and Nutrition, Nara Women's University, Nara 630-8506, Japan.
Abstract:
A significant increase in plasma glutamate-oxaloacetate transaminase and glutamate-pyruvate transaminase was observed 6 h after intraperitoneal administration of D-galactosamine (D-Galn). Three hours after administration of D-Galn, the vitamin C concentration in the liver decreased significantly compared to that in a control group and thereafter the hepatic vitamin C concentration remained at a significantly lower level. Phosphorylated JNK (c-Jun NH2-terminal kinase) and phosphorylated ERK (extracellular signal-regulated kinase) started increasing 3 h after D-Galn treatment and remained at a high level for 6-12 h after the treatment, while phosphorylated p38 MAPK increased significantly 6 h after D-Galn administration. These results indicated that oxidative stress and the activation of JNK and ERK took place almost simultaneously, followed by the activation of p38 MAPK.
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