摘要
目的 观察灵芝三萜类成分TG和TG2 在体内外对小鼠免疫性肝损伤的影响。方法 制备BCG +LPS引起的小鼠免疫性肝损伤模型 ,并采用小鼠肝细胞原代培养方法 ,取血清和细胞上清测定其中ALT ,NO和肝脏TG水平并进行肝脏病理组织检查。结果 体内实验表明GT 80mg·kg-1和GT2 10 ,2 0 ,40mg·kg-1均明显降低模型动物的血清ALT ,NO和肝脏TG含量 ,并不同程度地减轻动物肝损伤程度。小鼠免疫性肝损伤后原代培养肝细胞的实验中 ,正常小鼠肝细胞上清ALT和NO基本未见改变 ,BCG +LPS损伤后小鼠肝细胞上清ALT和NO在 12 ,2 4h较正常小鼠明显升高 ,并随时间的延长明显增高。而GT 0 .5 ,5 ,5 0 ,10 0 μg·ml-1和GT2 0 .5 ,2 ,10 ,5 0 μg·ml-1均程度不同地使升高的ALT和NO明显下降。灵芝三萜类 (GT ,GT2 )的以上作用与阳性对照药马洛替酯 (MaI)相似。结论 灵芝三萜类成分GT和GT2 对小鼠免疫性肝损伤有明显的保护作用。
OBJECTIVE To study the effects of triterpenoids isolated from Ganoderma lucidum (Leyss,ex Fr.) Karst. on immunological liver injury model in mice and in vitro .METHODS Bacillus Calmette Guerin plus lipopolysaccharides were used to induce immunological liver injury in mice.The primary mouse hepatocytes were separated and cultured with the test compounds.Seurm and the supernatant of cells after 3~24 h incubation were taken for the estimation of ALT,nitric oxide (NO) and liver triglycerid (TG) respectively.The histopathologic change in the liver of mice was observed.RESULTS In vivo, GT(80 mg·kg -1 ) and GT 2 (10,20,40 mg·kg -1 ) were found to significantly inhibit the increase of serum ALT,NO and liver TG levels induced by BCG plus LPS,and improve the liver injury in different degree. In vitro, ALT and NO in the supernatant of the normal mouse hepatocytes had no significant changes in 24 h.Whereas ALT and NO of the BCG+LPS group were increased within 12 h and 24 h in a dependent manner.GT(0.5,5,50,100 μg·ml -1 ) and GT 2(0.5,2,10,50 μg·ml -1 ) decreased ALT and NO in different degree.The mentioned above effects of GT and GT 2 were similar with those of malotilate.CONCLUSION The results indicate that the triterpenoids from Ganoderma lucidum (Leyss.ex.Fr.)Karst. had significant protective effects against immunological liver damage induced by BCG plus LPS in mice both in vivo and in vitro.
出处
《中国药学杂志》
CAS
CSCD
北大核心
2000年第12期809-812,共4页
Chinese Pharmaceutical Journal
关键词
灵芝
三萜
免疫性肝损伤
肝细胞
小鼠
中药
Ganoderma lucidum (Leyss.ex Fr.) Karst.
triterpenoids
immunological liver injury
hepatocyteH