阿魏酸钠的抗肝损伤作用及其机制研究

目的: 研究阿魏酸钠(SF)的抗CCl4 肝损伤作用及其作用机制。方法: 以血清ALT 、AST 为诊断指标, 建立急性肝损伤模型, 测定肝细胞浆抗氧化酶、肝线粒体ATP 酶和膜流动性。结果: CCl4 致小鼠血清ALT 和AST 升高时, 单胺氧化酶显著升高, 过氧化氢酶、谷胱甘肽S-转移酶(GST)及膜荧光偏振度、平均微粘度显著降低, Na⁺, K⁺-ATP 酶、Ca²⁺,Mg²⁺-ATP 酶活性呈降低趋势。预先给予SF 50 ~150 mg·kg^-1 (ip, qd ×9)后能明显逆转上述改变, 并呈剂量依赖性变化。结论: SF 对CCl4 肝损伤有保护作用。其作用机制除抑制脂质过氧化作用外, 还与增强肝GSH 结合功能, 保护线粒体膜结构和功能有关。

Protection and mechanism of sodium ferulate on CCl4-induced liver injury in mice

AIM: To study the protective efficacy and mechanism of sodium ferulate on CCl4-induced liver injury in mice.METHODS: CCl4-induced acute liver injury model was made in mice.Serum levels of alanine aminotransferase (ALT)and aspartate aminotransferase (AST) criteria, activities of catalase (Cat), glutathione S-transferase (GST), monoamine oxidase (MAO), Na⁺, K⁺-ATPase, Ca²⁺, Mg²⁺-ATPase and membrane fluidity in liver cytosol and mitochondrion were measured.RESULTS: Based on the condition that serum levels of ALT and AST increased in mice induced by CCl4, the activity of mitochondrional MAO significantly increased, and the activities of cytosol Cat and GST, the values of mitochondria fluorescence polarization, and mean microviscosity decreased.Meanwhile, the activities of Na⁺, K⁺- and Ca²⁺, Mg²⁺-ATP ase showed the increasing tendency. Pretreatment with sodium ferulate (50-150 mg·kg^-1 ip, qd ×9)could inverse these alterations above obviously, and showed the dose-dependent changes.CONCLUSION: The hepatic-protective action of sodium ferulate may be related with the reinforcement of liver glutathione conjugation catalyzed by GST, the recoveries of mitochondria membrane fluidity and ATPase activities as well as its antioxidative effect.