Muriel P, Mourelle M
Departamento de Farmacologia y Toxicología, Centro de Investigación yde Estudios Avanzados del Instituto Politécnico Nacional, Mexico, D.F.
J Appl Toxicol. 1990 Aug;10(4):275-9. doi: 10.1002/jat.2550100408.
The effect of silymarin on liver lipid peroxidation and membrane lipid alterations induced by an acute dose of CCl4 was studied. Four groups of animals were treated with CCl4, CCl4 + silymarin, silymarin and its vehicles. CCl4 was given orally (0.4 g 100 g-1 body wt.) and silymarin was administered i.p. All animals were sacrificed 24 h after the treatments. Liver lipid peroxidation was measured and plasma membranes were isolated. Alkaline phosphatase (AP) and gamma-glutamyl transpeptidase (GGTP) were measured in plasma membranes. Membrane lipids were extracted and then analysed by thin-layer chromatography by measuring the phosphorus of the phospholipids in each spot. Liver lipid peroxidation was increased about three times in the group receiving CCl4 only. Silymarin cotreatment prevented this increase. Phosphatidylethanolamine (PEA) decreased, while phosphatidylinositol (PI) increased in the plasma membranes isolated from the CCl4-treated group. Animals that received CCl4 + silymarin showed no decrease in PEA content. A partial prevention of the decrease in phosphatidylinositol content was also observed in plasma membranes of animals treated with silymarin in addition to CCl4. CCl4 decreased gamma-glutamyl transpeptidase (GGTP) and alkaline phosphatase (AP) membrane activities. Silymarin cotreatment prevented the AP (completely) and the GGTP (partially) falls caused by CCl4. Silymarin by itself increased AP membrane activity. A significant relationship between the membrane content of phosphatidylethanolamine (PEA) and the AP activity was observed in plasma membranes of treated animals and in normal liver membranes enriched with PEA. These results indicate that silymarin can protect against the alterations induced by CCl4 on the liver plasma membrane through its antioxidant properties by modifying the plasma membrane phospholipid content.
研究了水飞蓟素对急性剂量四氯化碳诱导的肝脏脂质过氧化和膜脂质改变的影响。将四组动物分别用四氯化碳、四氯化碳 + 水飞蓟素、水飞蓟素及其赋形剂进行处理。四氯化碳经口给予(0.4 g/100 g体重),水飞蓟素经腹腔注射。处理24小时后处死所有动物。测定肝脏脂质过氧化水平并分离质膜。测定质膜中的碱性磷酸酶(AP)和γ-谷氨酰转肽酶(GGTP)。提取膜脂质,然后通过测量每个斑点中磷脂的磷含量,采用薄层色谱法进行分析。仅接受四氯化碳处理的组中,肝脏脂质过氧化增加了约三倍。水飞蓟素联合处理可防止这种增加。从四氯化碳处理组分离的质膜中,磷脂酰乙醇胺(PEA)减少,而磷脂酰肌醇(PI)增加。接受四氯化碳 + 水飞蓟素处理的动物中,PEA含量没有降低。在除四氯化碳外还用水飞蓟素处理的动物的质膜中,也观察到磷脂酰肌醇含量降低得到部分预防。四氯化碳降低了γ-谷氨酰转肽酶(GGTP)和碱性磷酸酶(AP)的膜活性。水飞蓟素联合处理可防止四氯化碳引起的AP(完全)和GGTP(部分)活性下降。水飞蓟素本身增加了AP膜活性。在处理动物的质膜和富含PEA的正常肝膜中,观察到磷脂酰乙醇胺(PEA)的膜含量与AP活性之间存在显著关系。这些结果表明,水飞蓟素可通过其抗氧化特性,通过改变质膜磷脂含量,保护肝脏质膜免受四氯化碳诱导的改变。