Muriel P, Suarez O R
Departamento de Farmacologia y Toxicologia, Del Instituto Politecnico Nacional Apartado Postal 14-740, Mexico, D.F., Mexico.
J Appl Toxicol. 1994 Nov-Dec;14(6):423-6. doi: 10.1002/jat.2550140607.
There is poor evidence about the participation of lipoperoxidative processes in liver damage induced by biliary obstruction, thus the aim of this work was to study the role of lipid peroxidation in this model of liver injury. Biliary obstruction was induced in male Wistar rats by ligation of the common bile duct; control animals were sham operated. Rats were sacrificed at different times after surgery. Liver sections were used for glycogen and lipoperoxidation quantification. Markers of liver damage were determined in serum. All serum markers of liver damage increased after 1 day of biliary obstruction. Liver glycogen content decreased 1 day after surgery. On the other hand, lipoperoxidation increased later than markers of liver damage, suggesting that it is a consequence rather than the cause of liver injury. Moreover, administration of colchiceine (a good free-radical scavenger) or vitamin E prevented lipoperoxidation but not liver damage, confirming that lipoperoxidation does not play an important role in liver damage induced by biliary obstruction. This model of liver injury seems to be useful for testing hepatoprotective drugs that do not act as free-radical scavengers.
关于脂过氧化过程参与胆汁梗阻所致肝损伤的证据不足，因此本研究的目的是探讨脂质过氧化在该肝损伤模型中的作用。通过结扎胆总管在雄性Wistar大鼠中诱导胆汁梗阻；对照动物进行假手术。术后在不同时间处死大鼠。肝组织切片用于糖原和脂质过氧化定量分析。测定血清中肝损伤标志物。胆汁梗阻1天后，所有肝损伤血清标志物均升高。术后1天肝糖原含量降低。另一方面，脂质过氧化的增加晚于肝损伤标志物，这表明它是肝损伤的结果而非原因。此外，给予秋水仙碱（一种良好的自由基清除剂）或维生素E可预防脂质过氧化，但不能预防肝损伤，这证实脂质过氧化在胆汁梗阻所致肝损伤中不发挥重要作用。这种肝损伤模型似乎有助于测试不作为自由基清除剂起作用的肝保护药物。
