Orthogonal design based optimization of a mouse model of acute liver failure induced by D-galactosamine and lipopolysaccharide.
- VernacularTitle:D-半乳糖胺/脂多糖所致小鼠急性肝衰竭模型正交试验优化研究
- Author:
Hao-zhen YANG
1
;
Long CHEN
;
Jing-jing TONG
;
Hui-ying ZHANG
;
Fei PANG
;
Zhi-heng XU
;
Shao-jie XIN
;
Jin-hua HU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Disease Models, Animal; Galactosamine; adverse effects; Lipopolysaccharides; adverse effects; Liver Failure, Acute; chemically induced; Male; Mice; Mice, Inbred C57BL
- From: Chinese Journal of Hepatology 2013;21(6):464-466
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo apply an orthogonal design optimization strategy to a mouse model of acute liver failure induced by D-galactosamine (D-GalN) and lipopolysaccharide (LPS) exposure.
METHODSA four-level orthogonal array design (L16(45)) was constructed to test factors with potential impact on successful establishment of the model (D-GalN and LPS dosages, and dilution rate of the D-GalN/LPS mixture). The mortality rate of mice within 24 hours of D-GalN/LPS administration was determined by the Kaplan-Meier method. The model outcome was verified by changes in serum alanine transferase level, liver histology, and hepatocyte apoptosis.
RESULTSThe orthogonal array identified the optimal model technique as intraperitoneal injection of a combination of D-GalN and LPS at dosages of 350 mg/kg and 30 mug/kg, respectively, and using a dilution rate of 3. The dosages tested had no effect on survival. The typical signs of liver failure appeared at 6 hrs after administration of the D-GalN/LPS combination.
CONCLUSIONThe orthogonal design optimization strategy provided a procedure for establishing a mouse model of acute liver failure induced by D-GalN and LPS that showed appropriate disease outcome and survival, and which will serve to improve future experimental research of acute liver failure.