吴茱萸水提组分多次给药致小鼠肝毒性氧化损伤机制研究

The research of oxidative damage mechanism on hepatic toxicity caused by water extraction components of Evodia Fructus to mice

目的:观察连续给予吴茱萸水提组分导致小鼠肝毒性损伤与氧化损伤机制的相关性。方法:吴茱萸水提组分5.0,2.5,0.63 g/kg,连续给药7天,检测血和肝组织内丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性、一氧化氮(NO)、一氧化氮合酶(NOS)、谷胱甘肽(GSH)和谷胱甘肽过氧化物酶(GSH-Px)的含量和活性。结果:吴茱萸水提组分在0.63～5.0 g/kg剂量范围内可致血中和肝组织内MDA含量增加,同时SOD活性下降;血和肝组织中一氧化氮(NO)含量增加,一氧化氮合酶(NOS)活性升高;血和肝组织中谷胱甘肽(GSH)含量下降,谷胱甘肽过氧化物酶(GSH-Px)活性下降。上述变化趋势随剂量增加而加重,与空白对照组比较有明显差异。结论:连续给小鼠灌服一定剂量的吴茱萸水提组分可致小鼠肝毒性损伤,其损伤途径与引起机体氧化应激后诱导脂质过氧化有关。

Objective：To investigate the relationship of oxidative damage mechanism in hepatic toxicity caused by water extraction components of Evodia Fructus to mice.Methods：The high,middle and low dose group were separately set 5.0,2.5,0.63 g/kg,mice were administrated with water extraction components of Evodia Fructus according to 7 days toxicity test method.The level of MDA、SOD、NO、NOS、GSH、GSH-Px in serum and hepatic tissue were detected.Results：The water extraction components of Evodia Fructus could cause the activity of MDA in serum and liver increased,the activity of SOD decreased;the level of NO and NOS were increased,and the activity of GSH and GSH-Px were decreased.All the changes were aggravated in accordance with the dosages.Conclusion：The continuous administration of water extraction components of Evodia Fructus to mice could induce obvious hepatotoxicity damage;the approach of hepatic damage was related with the peroxidative damage mechanism.