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S-腺苷甲硫氨酸治疗可预防四氯化碳诱导的S-腺苷甲硫氨酸合成酶失活,并减轻肝损伤。

S-adenosylmethionine treatment prevents carbon tetrachloride-induced S-adenosylmethionine synthetase inactivation and attenuates liver injury.

作者信息

Corrales F, Giménez A, Alvarez L, Caballería J, Pajares M A, Andreu H, Parés A, Mato J M, Rodés J

机构信息

Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Cientificas, Madrid, Spain.

出版信息

Hepatology. 1992 Oct;16(4):1022-7. doi: 10.1002/hep.1840160427.

DOI:10.1002/hep.1840160427
PMID:1398482
Abstract

Administration of carbon tetrachloride to rats resulted in induction of hepatic fibrosis and a 60% reduction of hepatic S-adenosylmethionine synthetase activity without producing any significant modification of hepatic levels of S-adenosylmethionine synthetase messenger RNA. The reduction of S-adenosylmethionine synthetase activity was corrected by treatment with S-adenosylmethionine (3 mg/kg/day, intramuscularly). Administration of carbon tetrachloride also produced a 45% depletion of liver glutathione (reduced form) that was corrected by S-adenosylmethionine treatment. After the rats received carbon tetrachloride, a 2.3-fold increase in liver collagen was observed; prolyl hydroxylase activity was 2.5 times greater than that seen in controls. These increases were attenuated in animals treated with carbon tetrachloride and S-adenosylmethionine. The attenuation by S-adenosylmethionine treatment of the fibrogenic effect of carbon tetrachloride was associated with a decrease in the number of rats in which cirrhosis developed.

摘要

给大鼠注射四氯化碳会导致肝纤维化,肝 S -腺苷甲硫氨酸合成酶活性降低 60%,而肝 S -腺苷甲硫氨酸合成酶信使核糖核酸水平未发生任何显著变化。用 S -腺苷甲硫氨酸(3 毫克/千克/天,肌肉注射)治疗可纠正 S -腺苷甲硫氨酸合成酶活性的降低。注射四氯化碳还会使肝脏谷胱甘肽(还原型)耗竭 45%,而 S -腺苷甲硫氨酸治疗可纠正这一情况。大鼠接受四氯化碳后,肝脏胶原蛋白增加了 2.3 倍;脯氨酰羟化酶活性比对照组高 2.5 倍。在用四氯化碳和 S -腺苷甲硫氨酸治疗的动物中,这些增加有所减弱。S -腺苷甲硫氨酸治疗对四氯化碳纤维化作用的减弱与肝硬化发生大鼠数量的减少有关。

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