黄药子对小鼠肝脏毒性的表达及其机理研究

目的 :探讨黄药子肝毒作用的指标和肝脏毒性产生的机理。方法 :黄药子 2g kg·d、10g kg·d、5 0g kg·d给予小鼠 ,连续给药 2 1d ,观察其生化指标变化 ,药物代谢酶及抗氧化酶活性及病理变化。结果 :黄药子可引起小鼠GPT、GOT、ALP、TBIL值增高 ,GST、GSH PX、SOD活力降低 ,且呈一定剂量、时间相关性。病理变化可见肝细胞疏松、肿胀、胞核溶解、融合、坏死、汇管区炎细胞浸润 ,小胆管水肿、增生等。其毒性产生与抑制GST、GSH PX、SOD等酶的活性有关。结论 :黄药子的肝毒作用客观化指标为GPT、GOT、ATP、TBIL及组织学变化。其毒性产生的机理与抑制肝微粒体中抗氧化酶和药物代谢酶活性有关。

The Express and Principle Study of Liver Toxicity of Dioscorea bulbifera L

Objective:To discuss the indexes and principle of Dioscorea bulbifera L liver toxicity.Method: Dioscorea bulbifera L, 2g/kg d,10g/kg d,50g/kg d were given to mice which lasted 21 days,and observe the change of biochemical indexes,the activity of medicine metabolizability enzyme and anti oxidation enzyme and pathology results.Result: Dioscorea bulbifera L can increase the GPT,GOT,ATP and TBIL levels and decrease the GST,GSH and SOD activity in mice,both of which is relevant to time and dosage.The pathology changes included looseness,tumidness,karyon dissolution,amalgamation,putrescence,confluent hepatic duct district inflammatory cells corrasion and small bile duct edema and hyperplasia.Conclusion:The indexes of Dioscorea bulbifera L toxicity are GPT,GOT,ATP,TBIL and tissue changes.The principle of toxicity is relevant to its inhibition of the activity of medicine metabolizability enzyme and anti oxidation enzyme in liver mitochondria.