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丹皮总苷对化学性肝损伤保护作用机制
引用本文:梅俏,魏伟,许建明,丁长海,能祖应,徐叔云.丹皮总苷对化学性肝损伤保护作用机制[J].中国药理学通报,1999,15(2).
作者姓名:梅俏  魏伟  许建明  丁长海  能祖应  徐叔云
作者单位:安徽医科大学临床药理研究所
基金项目:安徽省“八五”攻关课题
摘    要:目的研究丹皮总苷(totalglucosidesofmuoltancortes,TGM)对CCl4和D Gal N致小鼠化学性肝损伤的保护作用机制。方法采用CCl4和D Gal N所致小鼠化学性肝损伤模型进行研究,用TBA法和DTNB法测定MDA和GSH Px。结果TGM具有促进肝脏糖原合成和提高血清蛋白含量的作用(P<001),可明显降低肝匀浆脂质过氧化产物丙二醛(MDA)的含量(P<001)及提高血清和肝脏谷胱甘肽过氧化物酶活力(P<001),且可缩短CCl4中毒小鼠ip戊巴比妥钠后的睡眠时间(P<001)。结论TGM可能通过影响肝脏代谢机能,增强抗氧化作用,加强解毒能力机制发挥抗损伤作用。

关 键 词:丹皮总苷  四氧化碳  D-氨基半乳糖  化学性肝损伤  脂质过氧化

The mechanisms of total glucosides of mudan cortex against chemical liver injury in mice
MEI Qiao,WEI Wei,XU JianMing,DING ChangHai,XIONG ZuYing,XU ShuYun.The mechanisms of total glucosides of mudan cortex against chemical liver injury in mice[J].Chinese Pharmacological Bulletin,1999,15(2).
Authors:MEI Qiao  WEI Wei  XU JianMing  DING ChangHai  XIONG ZuYing  XU ShuYun
Abstract:AIM To study the protective mechanism of total glucosides of mudan cortex on liver injury produced by CCl4 and DGalN in mice. METHODS The mouse liver injury model was produced by CCl4 and DGalN, the content of MDA and GSHPx in the livers were measured. RESULTS The serum protein and hepatic glycogen content were improved, the molondialdehyde (MDA) content in hepatic homogenate was decreased, the glutathione peroxidase (GSHPx) activity was elevated in serum and liver in mouse by pretreatment with TGM, the sleeping time induced by sodium phenobarbital in the toxicated mice was reduced by TGM. CONCLUSION TGM had protective effects on chemical liver injury by promoting hepatocyte metabolism, enhancing antioxidation and antitoxic activity in liver.
Keywords:total glucosides of mudan cortex  CCl4  DGalN  chemical liver injury  lipidperoxide (LPO)  
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