PREVENTION BY SILYMARIN OF MEMBRANE-ALTERATIONS IN ACUTE CCL4 LIVER-DAMAGE
PREVENTION BY SILYMARIN OF MEMBRANE-ALTERATIONS IN ACUTE CCL4 LIVER-DAMAGE
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DOI：
10.1002/jat.2550100408
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发表时间：
1990-08-01
影响因子：
3.3
通讯作者：
MOURELLE, M
中科院分区：
文献类型：
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作者：
MURIEL, P;MOURELLE, M
研究了水飞蓟素对急性剂量CCl4所致大鼠肝脏脂质过氧化和膜脂改变的影响。分别用CCl_4、CCl_4+水飞蓟素、水飞蓟素及其载体处理4组动物。口服CCl4(0.4g，100g-1体重)。水飞蓟素接受了ip。治疗后24小时处死动物。测定肝脏脂质过氧化反应，分离质膜。测定细胞质膜碱性磷酸酶(AP)和γ-谷氨酰转肽酶(GGTP)活性。提取膜脂，用薄层层析法测定各点磷脂的磷含量。在仅接受CCl4的组中，肝脏的脂质过氧化反应增加了约三倍。水飞蓟素共治疗阻止了这种增加。CCl4处理组分离的细胞膜磷脂酰乙醇胺(PEA)减少，磷脂酰肌醇(PI)增加。接受CCl4+水飞蓟素的动物在PEA含量上没有下降。水飞蓟素加CCl4处理的动物的细胞膜中磷脂酰肌醇含量的下降也被观察到部分阻止。CCl4降低了γ-谷氨酰转肽酶(GGTP)和碱性磷酸酶(AP)的膜活性。水飞蓟素联合治疗可完全阻止CCl_4引起的AP和GGTP的下降。水飞蓟素本身可增加AP膜的活性。磷脂酰乙醇胺(PEA)的膜含量与AP活性之间存在显著的相关性。这些结果表明，水飞蓟素可能通过改变肝细胞质膜磷脂含量来对抗CCl4对肝细胞质膜的损伤。
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.