Iida Chinatsu, Fujii Kozue, Koga Eriko, Washino Yukiko, Ichi Ikuyo, Kojo Shosuke
Department of Food Science and Nutrition, Nara Women's University, Nara 630-8506, Japan.
J Nutr Sci Vitaminol (Tokyo). 2007 Apr;53(2):160-5. doi: 10.3177/jnsv.53.160.
D-Galactosamine (D-Galn: 300 mg/kg) was intraperitoneally administered to rats. After 6 h the activity of plasma GOT and GPT was significantly higher than that of the control group and plasma GOT and GPT activities increased thereafter. These results indicated that the necrotic process was initiated at about 6 h and developed thereafter. With coadministration of DMSO (1 h before administration of D-Galn: 2.5 mL/kg, oral), plasma GOT and GPT were significantly lower, showing that DMSO inhibited the necrotic action of D-Galn. After 6-24 h of D-Galn administration, the hepatic level of vitamin C, the most sensitive indicator of oxidative stress, decreased significantly, indicating that oxidative stress was significantly enhanced 6 h after D-Galn intoxication and thereafter. DMSO significantly restored the liver vitamin C level 24 h after D-Galn injection, demonstrating that DMSO effectively ameliorated the oxidative stress caused by D-Galn, resulting in the prevention of necrosis of the liver. Phosphorylated JNK and phospho-ERK were significantly increased transiently 6-12 h after treatment with D-Galn. These results indicated that oxidative stress and the activation of JNK took place almost simultaneously. Phosphorylated p38 MAPK was not changed and DMSO treatment did not affect the change of these MAPKs by D-Galn.
将D-半乳糖胺（D-Galn：300毫克/千克）腹腔注射给大鼠。6小时后，血浆谷草转氨酶（GOT）和谷丙转氨酶（GPT）的活性显著高于对照组，此后血浆GOT和GPT活性持续升高。这些结果表明坏死过程在约6小时开始并随后发展。同时给予二甲基亚砜（DMSO，在给予D-Galn前1小时：2.5毫升/千克，口服），血浆GOT和GPT显著降低，表明DMSO抑制了D-Galn的坏死作用。给予D-Galn 6-24小时后，氧化应激最敏感指标肝内维生素C水平显著下降，表明D-Galn中毒6小时后及此后氧化应激显著增强。DMSO在D-Galn注射24小时后显著恢复了肝脏维生素C水平，表明DMSO有效改善了D-Galn引起的氧化应激，从而预防了肝脏坏死。用D-Galn处理6-12小时后，磷酸化JNK和磷酸化ERK短暂显著增加。这些结果表明氧化应激和JNK的激活几乎同时发生。磷酸化p38丝裂原活化蛋白激酶（p38 MAPK）没有变化，DMSO处理不影响D-Galn引起的这些丝裂原活化蛋白激酶的变化。
