吴茱萸挥发油多次给药致小鼠肝毒性氧化损伤机制研究

摘要

目的：观察连续给予吴茱萸挥发油导致小鼠肝毒性损伤程度与氧化损伤的相关性。方法小鼠按照吴茱萸挥发油高、中、低剂量分别为1.25、1.0、0.25 mL·kg-1，连续给药7天，每天灌胃给药1次，7天后检测血和肝组织内丙二醛（MDA）水平和超氧化物歧化酶（SOD）活性，谷胱甘肽（GSH）、一氧化氮（NO）含量和谷胱甘肽过氧化物酶（GSH-Px）、一氧化氮合酶（NOS）的活性。结果吴茱萸挥发油可致血和肝组织内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。结论吴茱萸挥发油多次给药后可导致小鼠肝毒性损伤，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 on hepatic toxic injury caused by volatile oil from Evodia Fructus in mice. Methods Mice were administrated with volatile oil from Evodia Fructus for 7 days, and the high, middle and low dose groups were separately set 1.25, 1.0, 0.25 mL·kg-1. The level of MDA、SOD、NO、NOS、GSH、GSH-Px in serum and hepatic tissue were detected after administration of 7 d. Results The volatile oil from Evodia Fructus could cause the increased activity of MDA in serum and liver, reduced level of SOD, however, the level of NO and NOS were increased. In addition to the reduced activity of GSH and GSH-Px, all the changes were aggravated in accordance with the dosages. Conclusion The continuous administration of volatile oil from Evodia Fructus on mice can induce obvious hepato toxicity injury. The approach of hepatic damage is related with the peroxidative damage mechanism.