摘要
目的:观察F1013对D-氨基半乳糖(D-GalN)及脂多糖(LPS)所致大鼠急性肝衰竭模型的保护作用,并对其机制进行初步探讨。方法:采用D-GalN/LPS诱导大鼠急性肝衰竭模型,用全自动生化分析仪检测血清ALT、AST和总胆红素(TBIL)含量;用苏木素-伊红(HE)染色,观察肝组织病理学变化;采用流式细胞学技术和原位末端标记(TUNEL)法检测肝细胞凋亡情况。结果:模型组大鼠血清ALT、AST、TBIL水平和肝细胞凋亡率较正常对照组均显著升高(P<0.01)。F1013(5,2.5,1.25 mg/kg)给药组大鼠肝组织病理损伤程度明显轻于模型组;血清ALT、AST水平和肝细胞凋亡率均较模型组明显降低(P<0.01或P<0.05),另F1013(5 mg/kg)给药组血清TBIL水平较模型组明显降低(P<0.01)。结论:F1013对GalN/LPS引起的大鼠急性肝衰竭有较好的保护作用,其机制可能与抑制肝细胞凋亡有关。
AIM：To observe the protective effect of F1013 on fulminant hepatic failure（FHF） induced by lipopolysaccharide（LPS） plus D-galactosamine（D-GalN） in rats and to investigate its mechanism of action. METHODS：The rat model of FHF was induced by intra-peritoneal injection of LPS plus D-GalN.The contents of ALT,AST and total bilirubin（TBIL） were examined by an entire automatic biochemistry,the hepatic pathological changes were observed with hematoxylin-eosin（HE） stain,and the hepatocyte apoptosis was detected with FCM and TUNEL.RESULTS：Compared with the control group,serum levels of ALT,AST and TBIL and the expression of hepatocyte apoptosis in rats of the model group were significantly elevated（P0.01）.Compared with the model group,5,2.5,1.25 mg/kg F1013 treatment groups could effectively improve the hepatic tissue injury,reduce serum levels of ALT and AST and the expression of hepatocyte apoptosis（P0.01 or P0.05）,5 mg/kg F1013 treatment group reduce serum levels of TBIL（P0.01）.CONCLUSION：It is shown that F1013 has a promising protective effect on rats with FHF caused by LPS plus D-GaIN,and its mechanism is probably related to the inhibition of liver tissue cell apoptosis.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2010年第11期1229-1233,共5页
Chinese Journal of Clinical Pharmacology and Therapeutics
关键词
F1013
急性肝衰竭
凋亡
F1013
Fulminant hepatic failure
Apoptosis
