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Metabolic Dysfunction-Associated Steatohepatitis
MASH animal model

Metabolic Dysfunction-Associated Steatohepatitis (MASH) Animal Model

Phenotypic stability

Highly simulates human MASH characteristics.

Multi-criteria evaluation

Metabolism, inflammation, fibrosis

Widely applicable

Pharmacological Efficacy Evaluation/Mechanistic Studies

Data can be standardized.

Standardized pouring process, high repeatability

Psychiatric & neurological disease models

Introduction to the MASH Mouse Model

Metabolic dysfunction‑associated steatohepatitis (MASH, formerly known as non‑alcoholic steatohepatitis, NASH) is a subtype of non‑alcoholic fatty liver disease (NAFLD) and represents a progressive metabolic liver disorder. It is characterized by hepatic steatosis, inflammatory responses, hepatocellular injury, and fibrosis; if left unchecked, the condition may progress to cirrhosis and even lead to hepatocellular carcinoma. Obesity, insulin resistance, and type 2 diabetes markedly increase the risk of developing MASH and accelerate disease progression.

In response to the needs of drug development and mechanistic research

We can flexibly control the endpoint of model induction, offering MASH animal models with or without fibrosis. We also provide comprehensive downstream pathway‑specific analyses for these models, encompassing key targets in pathways such as AMPK/ACC, NF‑κB, and TGF‑β1/Smad, among others.

High-fidelity biological characteristics

To accurately model the critical steps in the progression from metabolic syndrome to liver cirrhosis, we employed the widely accepted composite diet–induced method. In addition to obvious phenotypic features such as a markedly rounded body shape, abdominal distension, and increased resistance to grasping, we established rigorous biochemical and metabolic reference standards.

High-fidelity biological characteristics

Advantages of Aniphe BioLabtechnology’s MASH Mouse Model Platform Services

Leveraging experience from thousands of MASH model‑building projects, we achieve a modeling success rate exceeding 95%. We implement rigorous in‑batch quality control and stringent inclusion criteria, providing a rapid and reliable in vivo solution for your drug discovery and preclinical efficacy evaluation.

● Model stability:Thousands of model‑building projects, with a success rate exceeding 95%.
● In‑batch quality control:Random sampling was used to assess body weight, four lipid parameters, and ultrasound elastography, ensuring phenotypic homogeneity prior to enrollment.
● Strictly selected for enrollment: Ensure that the body weight variation within each experimental batch is less than 10% to maintain statistical power.
● Predictive assessment of treatment efficacy:By employing a comprehensive disease‑progression model, it is possible to predict in advance the therapeutic efficacy of drugs across the distinct stages of inflammation, steatosis, and hepatic fibrosis, thereby reducing the rate of clinical trial failure.
● Fast and stable:A rapid and stable in vivo solution.

Experimental results

Establishment and Validation of a Diet-Induced MASH Mouse Model of Hepatic Injury

Metabolic abnormalities: Following the induction of the model by switching to a high-fat diet, blood glucose levels in the model group mice were significantly elevated. Intraperitoneal glucose tolerance testing (IPGTT) revealed that, even 2 hours after glucose administration, blood glucose remained above baseline, and the area under the curve was markedly larger than that of the control group mice.

Liver Injury and Lipid Metabolism Disorders: Serum biochemical assays revealed that, compared with the blank control group, the model‑group mice exhibited significantly elevated levels of ALT and AST, indicating marked hepatic damage. Concurrently, serum concentrations of TG, TC, LDL‑c, and HDL‑c were markedly increased relative to the blank control group, suggesting dyslipidemia in the NASH mice.

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Levels of TG, TC, LDL‑c, HDL‑c, ALT, and AST in the serum of mice from the NASH model group and the control group. Data are presented as Mean ± SD (n = 3). p* < 0.05, p** < 0.01, p*** < 0.001, p**** < 0.0001.

ZST+ Domain Light Ultrasound: Noninvasive Dynamic Monitoring of Drug Efficacy in Liver Fibrosis

Traditionally, assessing liver fibrosis has required end-point histological sampling, which not only consumes experimental animals but also precludes the acquisition of longitudinal data from individual mice before and after treatment. To address this limitation, we have implemented in vivo imaging using the ZST plus domain‑light high‑frequency animal ultrasound system. This platform leverages three core technologies to overcome the drawbacks of conventional linear scanning and manual pressure: domain‑scanning and domain‑processing harness the mouse’s intrinsic physiological pulsations to quantify tissue deformation, thereby minimizing human error; domain‑focusing is tailored to the mouse liver’s dimensions, enhancing imaging resolution; and, combined with natural strain elastography, it delivers objective, quantitative strain‑ratio measurements, enabling continuous, in vivo evaluation of hepatic stiffness with more robust and reliable data.

Ultrasound results showed that, as the modeling period progressed, the hardness histogram of the model group shifted significantly toward the high‑hardness (Hard) region, while the strain ratio increased markedly in a time‑dependent manner, objectively quantifying and reproducing the progressive pathological process of hepatic fibrosis. This not only closely corresponded to the collagen fiber deposition area assessed at the endpoint but also enabled researchers to dynamically monitor the effects of pharmacological interventions in real time, without sacrificing the animals.

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Evolution of Liver Stiffness on Ultrasound Elastography in MASH Mice from 16 to 36 Weeks of Age

Pathological gold standard at the endpoint: from qualitative observation to quantitative scoring

Whether the model was successfully established ultimately depends on the pathological gold standard. We performed a comprehensive series of histopathological analyses to validate the model mice:

H&E staining: In the model group, hepatocyte arrangement was disorganized, with numerous round vacuoles observed in the cytoplasm, and marked hepatocyte swelling and rounding (ballooning degeneration), reflecting typical hepatocellular injury and steatosis.

Oil Red O staining: Hepatocytes in the model group were filled with numerous, densely packed bright red lipid droplets, confirming severe steatosis.

Masson’s trichrome staining: In the model group, prominent blue‑stained deposits were observed in the hepatic cords and around the central veins, clearly confirming the development of hepatic fibrosis and indicating that the model has progressed to the fibrotic stage.

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Multiple pathological stains confirmed that NASH model mice exhibit features of steatosis and hepatic fibrosis.

Advanced Delivery Standards

In addition to intuitive histopathological images, we provide NAS‑based quantitative data that meet international standards—comprising assessments of steatosis, lobular inflammation, and ballooning—and perform rigorous fibrosis staging (F0–F4), thereby furnishing robust, statistically valid evidence for your pharmacological efficacy evaluations.

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The NAS scoring system consists of three components: ① hepatocellular steatosis (0–3 points); ② lobular inflammation (0–3 points); and ③ ballooning degeneration (0–2 points), with a total score ranging from 0 to 8. A NAS score <3 is classified as non‑NASH; a NAS score >4 is classified as NASH; and a NAS score between 3 and 4 indicates a possible diagnosis of NASH.