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Liver Diseases
Acute and chronic liver diseases are frequent and potentially life threatening for humans. The underlying etiologies are diverse, ranging from viral infections, autoimmune disorders, and intoxications to imbalanced diets and others. Therefore, animal liver disease models are in needs to mimic human liver diseases. HD Biosciences has established multiple animal liver disease models including acute liver injury; obesity related liver damage; nonalcoholic steatohepatitis (NASH); alcoholic steatohepatitis (ASH), liver fibrosis, liver cirrhosis and hepatocellular carcinoma (HCC). These models possess distinct features and etiology of human liver diseases to help evaluate the efficacy of lead compounds in relevant clinical liver diseases and are designed for better understanding of underlying
mechanisms for new drugs to be used in clinic
In vitro biochemistry, cell-based and functional assays
MOA and functional analysis including evaluation of cell proliferation, cell apoptosis
and specific fibrogenic pathways
Characterization of markers involving in liver injury, fibrogenesis or fibrolysis at gene
and protein levels with qPCR, ELISA, western blot, LC/MS/MS, etc.
Human HSC LX-2, rat HSC T6, primary rodent HSC and hepatocyte systems
In vivo animal models
Acute liver injury models
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Alcohol induced acute liver injury in Kunming mouse & non human primate (NHP)
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CCl4 induced acute liver injury in rodents & NHP
Chronic fatty liver models
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Obesity in liver damage rodent models
HFD-induced fatty liver in mice and rats
ob/ob mice, db/db mice with fatty liver
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Obesity and liver damage in NHP model
HFD-induced fatty liver in cynomolgus monkeys
Chronic liver injury models
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Liver fibrosis/cirrhosis models
CCl4 induced liver fibrosis (mice, rats)
CCl4 induced liver cirrhosis (mice, rats)
Bile duct ligation (BDL) induced liver fibrosis (mice, rats)
Fatty liver + CCl4 induced liver fibrosis (mice, rats, NHP)
Fatty liver + CCl4 induced liver cirrhosis (mice, rats)
Alcohol induced chronic liver damage (NHP)
Non Alcoholic steatohepatitis (NASH) / HCC models
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Fatty liver with NASH model
DIO + CCl4 induced NASH in mice
DIO + CCl4 induced NASH in NHP
STZ + HFD induced NASH, fibrosis, cirrhosis and HCC in mice
Complicated factor induced chronic liver injury model
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High fat diet+alcohol+CCl4 induced liver fibrosis in monkey model
Endpoint Measurement
Clinical observation and physical examination
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Body weight, behavior, food intake, water intake, defecation
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Liver weight and spleen weight, ascite measurement, portal vein pressure
Biomarker analysis
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Serum ALT / AST analysis
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Gene expression and profiling (RT-PCR, microarray gene expression, miRNA)
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Protein and metabolite profiling (WB, ELISA, mass spectrometry)
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Hepatic hydroxyproline detection
Histology analysis
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H&E staining in liver tissues
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Sirius red staining and Masson Trchrome staining for collagen deposition and quantification in liver tissue
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α-SMA IHC staining and quantification in liver tissues
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Other related IHC staining for focused targets and markers
Representative Data
Liver damage in obese mouse models
Figure 1: Severe fatty liver was observed in high fat diet (HFD) induced DIO mice.
Figure 2: Pathology Evaluation on Liver Fibrosis in Obese Mice (NASH) CHFD 20 weeks, CCl4 for 4 weeks. H&E: Hepatocyte balloon degeneration with portal area inflammatory cell infiltration. Sirius Red: Collagen deposition in portal and intra lobular area. PAS: Glycogen deposit in hepatocytes.
 
CCl4 induced chronic liver damage in mouse and rat models
Figure 3: CCl4 induced liver fibrosis model development in Balb/c mice, CCl4 0.5ul/g (1:5) i.p. twice a week for 8 weeks. Blood serum ALT and AST elevated significantly. Liver collagen deposition and myofibroblast proliferation have been detected.
Figure 4: Histological examination of CCl4 induced liver cirrhosis rat model. Inflammatory cell infiltration, hepatocyte degeneration, fibrosis and cirrhosis were observed.
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HD Biosciences (China) Co.,Ltd
590 Ruiqing Road
Zhangjiang East Campus, Pudong, Shanghai 201201,
P.R.China
Tel: +86 (21) 5116 3700
Fax: +86 (21) 5116 3766
info@hdbiosciences.com
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