Nonalcoholic Steatohepatitis (NASH) Models

Biocytogen has developed multiple metabolic dysfunction–associated steatohepatitis (MASH) mouse models, formerly known as nonalcoholic steatohepatitis (NASH) mouse models, to support preclinical MASH/NASH research and liver disease drug evaluation. Available models include the Gubra-Amylin (GAN) diet–induced MASH/NASH mouse model, GAN + CCL4–induced model, high-fat methionine choline–deficient (HFMCD) model, and STAM MASH/NASH mouse model. These MASH/NASH models reproduce key pathological features of human metabolic liver disease, including hepatic steatosis, inflammation, and fibrosis, providing reliable in vivo platforms for studying disease mechanisms and evaluating anti-steatotic, anti-inflammatory, and anti-fibrotic therapeutics.
Nonalcoholic Steatohepatitis (NASH) Models

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  • MASH/NASH Mouse Model Introduction
  • Results

Publication

    MASH/NASH Mouse Model Introduction

    Metabolic dysfunction–associated steatohepatitis (MASH), formerly known as nonalcoholic steatohepatitis (NASH), is a progressive metabolic liver disease within the nonalcoholic fatty liver disease (NAFLD) spectrum. It is characterized by hepatic steatosis, inflammation, hepatocyte injury, and fibrosis, which can progress to cirrhosis or hepatocellular carcinoma. The co-existence of obesity, insulin resistance, and type II diabetes significantly increases the risk of disease onset and progression.

    Clinically, MASH involves steatohepatitis, hepatocyte ballooning, liver fibrosis, and metabolic dysfunction. To better understand disease mechanisms and evaluate new treatments, MASH/NASH mouse models are widely used in preclinical liver disease research. These include genetically modified, diet-induced, or a combination of the two.

    Biocytogen has established several validated models representing different stages of MASH pathogenesis, including:

    • CCl₄-induced MASH model, characterized by liver inflammation and fibrosis.
    • Gubra-Amylin (GAN) diet–induced MASH mouse model, showing obesity, glucose intolerance, and hepatic steatosis.
    • High-fat methionine–choline-deficient (HFMCD) diet–induced MASH model, producing severe hepatic injury and fibrosis.
    • STAM model, in which neonatal mice treated with streptozotocin (STZ) and fed a high-fat diet develop steatohepatitis, hyperglycemia, and metabolic dysfunction.

    These MASH/NASH models provide reliable in vivo platforms for mechanistic studies, drug efficacy testing, and preclinical research, advancing the discovery of anti-steatotic, anti-inflammatory, and anti-fibrotic therapies.

    Results
    GAN diet+CCL4 Induced NASH Mouse Model
    GAN diet+CCL4 Induced NASH Mouse Model

    MGL3196 and OCA alleviated NASH symptom in GAN diet+CCL4 induced NASH mouse model. A-B, ALT and AST levels of modeling and treatment group. C-F, TG, TC, HDL-C, LDL-C levels of modeling and treatment group. Data are expressed as mean ± SEM. N = 9 mice per group. *p<0.05, **p<0.01,***p<0.001.

    Resmetirom and OCA treatment alleviates symptoms of NASH
    Resmetirom and OCA treatment alleviates symptoms of NASH

    Resmetirom and OCA decreased NAS scores. A, Representative pictures of H&E staining showing degree of NASH. B, NAFLD activity score (NAS) assessed by an external expert pathologist. C-D, TG and TC content in liver after treatment. Data are expressed as mean ± SEM. N = 9-10 mice per group. *p<0.05, **p<0.01, ***p<0.001.

    Resmetirom and OCA treatment alleviates liver fibrosis
    Resmetirom and OCA treatment alleviates liver fibrosis

    Resmetirom and OCA treatment alleviates liver fibrosis. A, Representative pictures of Sirius Red staining showing degree of liver fibrosis (scare bar: 200μm). B, Liver fibrosis score was assessed according to Sirius Red staining. C, Representative pictures of IHC staining showing α-SMA expression (scare bar: 200μm).D, Quantitively data of α-SMA expression. Data are expressed as mean ± SEM. N = 9 mice per group. *p<0.05, **p<0.01,***p<0.001,****p<0.0001.