Methods for Establishing and Evaluating Animal Models of Acute Liver Injury

Animal models of acute liver injury are used to simulate hepatocellular necrosis, inflammatory responses, oxidative stress, cholestasis, or metabolic disorders occurring within a short period of time. They are important experimental systems for studying mechanisms of liver injury, evaluating hepatoprotective agents, and screening intervention targets. Commonly used models include carbon tetrachloride-, acetaminophen-, concanavalin A-, D-galactosamine/lipopolysaccharide-, and ethanol-induced models. Different models differ in injury mechanism, modeling time, and evaluation indicators.

Keywords: acute liver injury; animal model; carbon tetrachloride; acetaminophen; concanavalin A; D-GalN/LPS; alcoholic liver injury; liver function indicators

1 Experimental Positioning of Animal Models of Acute Liver Injury

1.1 Objectives of Model Establishment

(1) Mechanistic studies

Acute liver injury models can be used to analyze hepatocellular necrosis, mitochondrial injury, oxidative stress, inflammatory factor release, immune cell activation, and abnormal bile excretion. Different inducers correspond to different pathological mechanisms. Therefore, the research focus should be clarified before selecting the modeling strategy.

(2) Pharmacodynamic evaluation

Screening of hepatoprotective drugs, antioxidants, anti-inflammatory agents, metabolic regulators, and natural products often requires stable acute liver injury models. If the injury is too mild, pharmacological effects may be difficult to distinguish; if the injury is too severe, animal mortality may increase or the therapeutic window may become too narrow. Therefore, preliminary experiments should be conducted before formal studies to determine the appropriate dose and sampling time.

(3) Indicator validation

Acute liver injury models can be used to validate detection systems for ALT, AST, LDH, total bilirubin, total bile acids, oxidative stress indicators, inflammatory factors, and pathological scoring. A single indicator usually cannot fully reflect the severity of liver injury; comprehensive evaluation should combine serum biochemistry, histopathology, and molecular mechanistic indicators.

1.2 Basis for Model Selection

(1) Matching injury mechanisms

Carbon tetrachloride is more suitable for studying free radical injury and lipid peroxidation. Acetaminophen is more suitable for simulating drug-induced liver injury. Concanavalin A is suitable for studies of T cell- and immune-mediated liver injury. D-GalN/LPS is suitable for studies of cytokine- and endotoxin-associated acute liver injury. Ethanol models are more suitable for research related to alcohol metabolism, lipid deposition, and oxidative stress.

(2) Observation time window

Acute liver injury is strongly time-dependent. In CCl4 and APAP models, marked serum transaminase elevation and pathological injury often appear within several hours to 24 h after administration. Inflammatory responses develop more rapidly in ConA and D-GalN/LPS models, whereas ethanol models are closely related to administration regimen, dose, and feeding status.

(3) Control of animal status

Animal strain, sex, age, body weight, fasting status, route of administration, and environmental stress can all affect model stability. APAP models are particularly affected by fasting and hepatic glutathione reserves, while immune-mediated models are more sensitive to animal immune status and the stability of tail vein injection.

Table 1 Key Points for Selecting Animal Models of Acute Liver Injury

Model Type	Representative Inducer	Main Mechanism	Modeling Characteristics	Suitable Research Directions
Chemical liver injury	Carbon tetrachloride	Free radical generation, lipid peroxidation, cell membrane injury	High modeling success rate and good reproducibility	Oxidative stress, hepatocellular necrosis, and liver repair
Drug-induced liver injury	Acetaminophen	NAPQI accumulation, GSH depletion, mitochondrial injury	Strong relevance to clinical drug-induced liver injury	Drug-induced liver injury, detoxification metabolism, and mitochondrial injury
T cell-mediated liver injury	Concanavalin A	T cell/NK cell activation and inflammatory factor release	Rapid inflammatory response with clear immune features	Immune hepatitis and T cell-mediated inflammation
Endotoxin-associated liver injury	D-GalN/LPS	Hepatocyte sensitization and TNF-α-mediated injury	Rapid modeling and marked inflammatory factor elevation	Endotoxemia, inflammatory factors, and mechanisms of liver failure
Alcoholic liver injury	Ethanol	Oxidative stress, lipid metabolism disorder, endotoxin translocation	Strongly dependent on administration regimen	Alcoholic liver injury, steatosis, and the gut-liver axis

2 Chemical and Drug-Induced Acute Liver Injury Models

2.1 Carbon Tetrachloride-Induced Model

(1) Injury mechanism

Carbon tetrachloride (CCl4) is a classical inducer of chemical liver injury. After metabolism by hepatic CYP enzyme systems, CCl4 generates trichloromethyl radicals and trichloromethyl peroxy radicals. These free radicals attack polyunsaturated fatty acids in cell and mitochondrial membranes, leading to lipid peroxidation, increased membrane permeability, calcium homeostasis disruption, and hepatocellular necrosis.

(2) Modeling points

CCl4 is usually diluted in vegetable oil or mineral oil before administration. It can be administered by intraperitoneal injection, oral gavage, subcutaneous injection, or other routes. Different administration routes correspond to different absorption rates and injury intensities. Acute models commonly use a single administration followed by short-term sampling, and are often used to observe serum ALT and AST elevation, hepatic necrosis, increased MDA, decreased GSH, and altered SOD activity.

(3) Applications and limitations

The CCl4 model is relatively simple to establish, has a high success rate, and shows good reproducibility. It is suitable for studies of oxidative stress, lipid peroxidation, hepatocellular necrosis, and injury repair. However, excessive model intensity may cause animal death or narrow the pharmacological observation window. If sampling is performed after the optimal time point, hepatic self-repair may affect the interpretation of ALT, AST, and pathological results.

2.2 Acetaminophen-Induced Model

(1) Injury mechanism

After overdose, acetaminophen (APAP) is metabolized in the liver by enzymes such as CYP2E1 to generate the highly reactive intermediate NAPQI. Under normal conditions, small amounts of NAPQI are cleared by glutathione. When GSH is depleted, NAPQI binds to mitochondrial proteins, causing mitochondrial oxidative stress, ATP depletion, and hepatocellular necrosis.

(2) Modeling points

The APAP model is commonly used to simulate drug-induced acute liver injury. Animal fasting status before administration, APAP dissolution conditions, dosage, route of administration, and sampling time all significantly influence model intensity. APAP has poor water solubility; therefore, preparation conditions should be kept stable, and freshly prepared solutions should be used whenever possible to reduce precipitation and dosing deviation.

(3) Applications and limitations

The APAP model is closely related to clinical drug-induced liver injury and is suitable for studying drug metabolism, GSH depletion, mitochondrial injury, necroinflammation, and detoxification interventions. This model is sensitive to fasting, sex, strain, and metabolic status. If these conditions are not controlled consistently, large intra-group variation may occur.

Table 2 Comparison of Chemical and Drug-Induced Acute Liver Injury Models

Model	Main Mechanism	Common Evaluation Indicators	Main Advantages	Main Limitations
CCl4 model	Free radical generation, lipid peroxidation, membrane injury	ALT, AST, MDA, SOD, GSH, hepatic necrosis	High modeling success rate; suitable for oxidative stress studies	Excessive dose may cause death; sampling time strongly affects results
APAP model	NAPQI accumulation, GSH depletion, mitochondrial injury	ALT, AST, GSH, MDA, mitochondrial injury, necrotic area	Strong relevance to drug-induced liver injury	Strongly affected by fasting, dissolution conditions, and metabolic status

3 Immune-Mediated Acute Liver Injury Models

3.1 Concanavalin A-Induced Model

(1) Injury mechanism

Concanavalin A (ConA) is a plant lectin that can activate T cells, NK cells, Kupffer cells, and multiple inflammatory pathways. It induces the release of inflammatory factors such as IFN-γ, TNF-α, and IL-6, and causes hepatocyte apoptosis or necrosis through immune cell-mediated inflammatory responses. This model is commonly used to study T cell-mediated hepatitis and mechanisms of immune liver injury.

(2) Modeling points

The ConA model is usually established by intravenous administration. Marked inflammatory responses and elevated transaminases can appear within a short time after administration. Model stability is influenced by animal strain, immune status, injection speed, solution condition, and tail vein injection technique. During experiments, operators and dosing conditions should be standardized as much as possible.

(3) Applications and limitations

The ConA model is suitable for studying immune cell activation, cytokine storm, T cell-mediated hepatitis, and evaluation of immunomodulatory drugs. This model requires relatively high technical proficiency in administration, and the inflammatory response progresses rapidly. Therefore, sampling time directly affects inflammatory factor levels, serum enzymology, and pathological findings.

3.2 D-GalN/LPS-Induced Model

(1) Injury mechanism

D-galactosamine (D-GalN) sensitizes hepatocytes to endotoxin, while lipopolysaccharide (LPS) activates TLR4-related inflammatory pathways and induces the release of cytokines such as TNF-α, IL-1β, and IL-6. Combined administration causes cytokine-mediated acute liver injury and is commonly used to simulate endotoxin-associated hepatitis and early processes of acute liver failure.

(2) Modeling points

The D-GalN/LPS model is usually established by combined administration, with rapid modeling and marked elevation of inflammatory factors. The ratio of D-GalN to LPS, administration timing, animal status, and sampling time should be carefully controlled. Preliminary experiments should be used to determine conditions that both produce stable injury and preserve a pharmacological evaluation window.

(3) Applications and limitations

This model is suitable for studying macrophage/Kupffer cell activation, TNF-α-mediated injury, inflammatory factor networks, and anti-inflammatory hepatoprotective drugs. If the model is too severe, mortality may increase, and excessive inflammatory responses may mask the protective effects of some interventions.

Table 3 Comparison of Immune-Mediated Acute Liver Injury Models

Model	Key Induction Process	Main Inflammatory Features	Common Indicators	Suitable Directions
ConA model	T cell/NK cell activation	Increased IFN-γ, TNF-α, and IL-6	ALT, AST, inflammatory factors, hepatic inflammatory infiltration	T cell-mediated hepatitis and immunomodulation studies
D-GalN/LPS model	Hepatocyte sensitization + endotoxin-induced inflammatory activation	Increased TNF-α, IL-1β, and IL-6	ALT, AST, TNF-α, IL-6, apoptosis/necrosis indicators	Endotoxin-associated liver injury, inflammatory factors, and acute liver failure studies

4 Alcoholic Acute Liver Injury Model

4.1 Ethanol-Induced Model

(1) Injury mechanism

Ethanol is mainly metabolized in the liver. Through pathways involving alcohol dehydrogenase, aldehyde dehydrogenase, and the microsomal ethanol-oxidizing system, ethanol generates acetaldehyde and reactive oxygen species, leading to oxidative stress, lipid metabolism disorder, triglyceride accumulation, and inflammatory responses. Ethanol can also increase intestinal permeability, allowing endotoxin to enter the portal venous system and activate Kupffer cells, thereby aggravating inflammatory liver injury.

(2) Modeling points

Acute ethanol-induced liver injury can be established by gavage, dietary intervention, injection, or other approaches. The specific regimen should be selected according to whether the study focuses on acute intoxication, steatosis, inflammatory response, or gut-liver axis alterations. Detection indicators may include ALT, AST, hepatic TG, MDA, GSH, inflammatory factors, and hepatic steatosis score.

(3) Applications and limitations

The ethanol model is suitable for studying alcohol metabolism, oxidative stress, steatosis, inflammatory injury, and gut-liver axis regulation. Results are strongly affected by diet, fasting, ethanol tolerance, administration route, and sampling time. If the research target is chronic alcoholic liver disease, longer-term dietary or chronic administration models should be used.

4.2 Differences Between Alcoholic Models and Other Models

(1) Injury characteristics

CCl4 and APAP models mainly involve toxic metabolites, free radicals, or mitochondrial injury. ConA and D-GalN/LPS models are dominated by immune-inflammatory responses. In contrast, ethanol models involve alcohol metabolism, oxidative stress, lipid deposition, and gut-derived endotoxin stimulation simultaneously. Model selection should therefore match the research question rather than be based only on modeling speed.

(2) Evaluation focus

In addition to ALT, AST, and pathological injury, ethanol models should place greater emphasis on hepatic lipid deposition, TG content, oxidative stress, inflammatory factors, and intestinal barrier-related indicators. If only transaminases are detected, the research value of steatosis and metabolic disorder in ethanol models may be underestimated.

Table 4 Application Comparison of Common Acute Liver Injury Models

Model Type	Representative Inducer	Main Pathological Features	Recommended Sampling Focus	More Suitable Research Question
Chemical liver injury	Carbon tetrachloride	Pericentral necrosis and lipid peroxidation	ALT, AST, MDA, SOD, GSH, pathological necrosis	Whether antioxidant and membrane-protective interventions are effective
Drug-induced liver injury	Acetaminophen	Mitochondrial injury, GSH depletion, hepatocellular necrosis	ALT, AST, GSH, mitochondrial injury, necrotic area	Whether drug toxicity and detoxification metabolism are regulated
T cell-mediated liver injury	Concanavalin A	Inflammatory infiltration and T cell-mediated necrosis	IFN-γ, TNF-α, IL-6, immune cell infiltration	Whether immune-inflammatory responses are suppressed
Endotoxin-associated liver injury	D-GalN/LPS	Elevated inflammatory factors and apoptosis/necrosis	TNF-α, IL-1β, IL-6, apoptosis indicators	Whether endotoxin inflammation and cytokine pathways are modulated
Alcoholic liver injury	Ethanol	Steatosis, oxidative stress, inflammatory response	TG, MDA, GSH, ALT, AST, steatosis score	Whether alcohol metabolism, lipid deposition, and the gut-liver axis are regulated

5 Evaluation Indicators and Quality Control

5.1 Serum Biochemical Indicators

(1) Transaminase indicators

ALT and AST are the most commonly used serum indicators for evaluating acute hepatocellular injury. ALT is more specific to hepatocellular injury, whereas AST can also be affected by mitochondrial injury, muscle sources, and systemic status. In acute injury models, elevated ALT and AST generally indicate impaired hepatocyte membrane integrity, but interpretation should be combined with pathology and the time window.

(2) Bilirubin and bile acid indicators

Total bilirubin, direct bilirubin, and total bile acids can be used to evaluate changes related to hepatobiliary excretion and cholestasis. Not all acute liver injury models produce obvious changes in bilirubin or bile acids. Whether these indicators should be included depends on the model mechanism and research objective.

5.2 Histopathology and Cell Death Indicators

(1) Pathological evaluation

HE staining can reveal hepatocyte swelling, necrosis, inflammatory infiltration, steatosis, and tissue architecture disruption, and is an important basis for evaluating acute liver injury models. In CCl4 and APAP models, necrotic areas and disruption of hepatic lobular architecture are commonly emphasized, whereas in ethanol models, steatosis and inflammatory changes should receive greater attention.

(2) Cell death

TUNEL, cleaved caspase-3, Bax/Bcl-2, HMGB1, and related indicators can be used to distinguish apoptosis, necrosis, or inflammatory cell death-related processes. D-GalN/LPS and ConA models are more suitable for combined evaluation of inflammatory factors and apoptosis indicators, whereas APAP models should focus more on necrosis and mitochondrial injury-related indicators.

5.3 Oxidative Stress and Inflammatory Indicators

(1) Oxidative stress

MDA, GSH, T-GSH, GSH-Px, SOD, and ROS levels can be used to evaluate oxidative injury and antioxidant defense capacity. CCl4, APAP, and ethanol models can all include oxidative stress indicators, but the timing and degree of oxidative stress differ among models and should be matched with the sampling time.

(2) Inflammatory factors

TNF-α, IL-1β, IL-6, IFN-γ, MCP-1, and related factors can be used to evaluate inflammatory responses. The ConA model places greater emphasis on T cell/NK cell-related inflammation, the D-GalN/LPS model focuses more on the endotoxin-induced TNF-α pathway, and the ethanol model can be analyzed together with gut-derived endotoxin and Kupffer cell activation.

Table 5 Common Evaluation Indicators for Acute Liver Injury Models

Indicator Category	Representative Indicators	Main Significance	Applicable Models
Liver function injury	ALT, AST, LDH	Hepatocyte membrane injury and enzyme release	All acute liver injury models
Bile excretion	TBIL, DBIL, TBA	Cholestasis and biliary excretory status	Cholestasis-related models and severe liver injury models
Oxidative stress	MDA, GSH, T-GSH, GSH-Px, SOD	Lipid peroxidation and antioxidant capacity	CCl4, APAP, and ethanol models
Inflammatory factors	TNF-α, IL-1β, IL-6, IFN-γ	Inflammatory response and immune activation	ConA, D-GalN/LPS, and ethanol models
Endotoxin response	LPS, LBP	Endotoxin exposure and gut-derived inflammatory response	D-GalN/LPS and ethanol models
Histopathology	HE staining, necrotic area, inflammation score, steatosis score	Tissue architecture and degree of pathological injury	All acute liver injury models
Cell death	TUNEL, cleaved caspase-3, Bax/Bcl-2, HMGB1	Apoptosis, necrosis, or inflammatory injury	APAP, ConA, and D-GalN/LPS models

6 Selection of Related Reagents and Materials

Table 6 Reagents Related to Establishing Animal Models of Acute Liver Injury

Cat. No.	Product Name	Grade & Purity	Model Type	Application Positioning
C639782	Carbon tetrachloride standard solution	analytical standard, ≥99.9%	CCl4 chemical liver injury model	Used to establish carbon tetrachloride-induced acute liver injury models; suitable for studies of oxidative stress, lipid peroxidation, and hepatocellular necrosis
A105808	4-Acetamidophenol	AR, ≥99%	APAP drug-induced liver injury model	Used to establish acetaminophen-induced drug-induced acute liver injury models
A105809	4-Acetamidophenol	analytical standard, ≥99.5%	APAP drug-induced liver injury model/standard	Suitable for APAP model-related method validation, dose control, and analytical standard use
A305928	4-Acetamidophenol	≥98%	APAP drug-induced liver injury model	Used for establishment of drug-induced liver injury models and APAP-related experimental systems
C491285	Concanavalin A lectin (Con A)	≥90%	ConA immune-mediated liver injury model	Used in ConA-induced acute immune liver injury experiments
G115553	D-(+)-Galactosamine hydrochloride	≥99%	D-GalN/LPS immune-inflammatory liver injury model	Used together with LPS to establish D-GalN/LPS-induced acute liver injury models
G115554	D-(+)-Galactosamine hydrochloride	for cell culture, ≥99%	D-GalN/LPS immune-inflammatory liver injury model	Used in D-GalN-related cellular or animal experimental systems
L1508370	Lipopolysaccharide (LPS) Solution (500X)	sterile-filtered,BioReagent,500X (1mg/mL)	D-GalN/LPS model/endotoxin stimulation	Used for LPS-related inflammatory stimulation, D-GalN/LPS models, or in vitro inflammatory validation
L384562	Lipopolysaccharides from Escherichia coli O111:B4	purified by phenol extraction	D-GalN/LPS model/endotoxin stimulation	Used for endotoxin-associated acute liver injury and inflammatory factor release studies
L386714	Lipopolysaccharide(LPS)	Derived from Escherichia coli 055:B5, purified by trichloroacetic acid extraction	D-GalN/LPS model/endotoxin stimulation	Suitable for LPS-induced inflammatory responses and D-GalN combined modeling
L755723	Lipopolysaccharides from Escherichia coli O127:B8	γ-irradiated, BioReagent, for cell culture	LPS inflammatory stimulation	Used for endotoxin inflammatory stimulation in cell culture systems
L755735	Lipopolysaccharides from Escherichia coli O26:B6	γ-irradiated, BioReagent, for cell culture	LPS inflammatory stimulation	Used for in vitro studies of Kupffer cells, macrophages, or inflammatory pathways

Table 7 Products for Evaluating Liver Function and Cholestasis in Acute Liver Injury

Cat. No.	Product Name	Grade & Purity	Indicator Category	Application Positioning
A1515821	Alanine Aminotransferase (ALT/GPT) Activity Assay Kit (DNPH, Micro Method)	BioReagent	Liver function injury	Used for ALT activity detection in serum, plasma, or tissue samples; a core indicator for evaluating acute hepatocellular injury
EJ1512755	Mouse Aspartate Aminotransferase (AST) ELISA Kit	BioReagent	Mouse AST detection	Used for AST-related detection in mouse acute liver injury models
EJ1514957	Human Aspartate Aminotransferase 2/Glutamic-oxaloacetic Transaminase 2 (AST2/GOT2) ELISA Kit	BioReagent	AST2/GOT2 detection	More suitable for human samples or mechanistic studies; not the preferred liver function indicator for mouse acute liver injury models
L1501786	Lactate Dehydrogenase (LDH) Cytotoxicity Assay Kit (DNPH, Micro Method)	BioReagent	Cell injury/cytotoxicity	Used for evaluating LDH release and cell membrane integrity damage
L1510342	Lactate Dehydrogenase (LDH) Activity Assay Kit (LD-L, Colorimetric Method)	BioReagent	LDH activity	Used for detecting LDH activity in serum, tissue, or cell samples
L1521751	Lactate Dehydrogenase (LDH) Activity Assay Kit (LD-P, UV Colorimetric Method)	BioReagent	LDH activity	Used for LDH activity detection in UV colorimetric systems
L1521750	Lactate Dehydrogenase (LDH) Cytotoxicity Assay Kit (DNPH, Colorimetric Method)	BioReagent	Cytotoxicity	Used for evaluating hepatocyte cytotoxicity, drug intervention, and cell injury
T1522116	Total Bilirubin (TBIL) Content Assay Kit (Micro Method)	BioReagent	Bilirubin metabolism/cholestasis	Used for total bilirubin detection; suitable for evaluation of severe acute liver injury and abnormal bile excretion
D1522115	Direct Bilirubin (DBIL) Content Assay Kit (Micro Method)	BioReagent	Direct bilirubin/bile excretion	Used for direct bilirubin detection; suitable for evaluating cholestasis, biliary excretory abnormalities, and severe liver injury
T1522089	Total Bile Acids (TBA) Content Assay Kit (Micro Method)	BioReagent	Bile acid metabolism/cholestasis	Used for total bile acid detection; suitable for evaluating hepatobiliary excretory abnormalities, cholestasis, and liver injury-related bile acid metabolism
U1509474	Urine Bilirubin Qualitative Detection Kit (Harrison's Method)	BioReagent	Urinary bilirubin	Used for auxiliary urine-based detection related to bile pigment metabolism; suitable for expanded evaluation of hepatobiliary excretory abnormalities

Table 8 Products for Evaluating Oxidative Stress, Inflammation, and Pathology in Acute Liver Injury

Cat. No.	Product Name	Grade & Purity	Indicator Category	Application Positioning
M1508248	Malondialdehyde (MDA) Content Assay Kit (TBA, Colorimetric Method)	BioReagent	Lipid peroxidation	Used for detecting hepatic MDA content in CCl4, APAP, ethanol, and other models
M1508267	Malondialdehyde (MDA) Content Assay Kit (TBA, Fluorometric Method)	BioReagent	Lipid peroxidation	Used for low-content samples or high-sensitivity MDA detection
L486287	Lipid Peroxidation (MDA) Assay Kit	sufficient for 100colorimetricorfluorometrictests	Lipid peroxidation	Used for detecting lipid oxidation levels; suitable for oxidative stress injury evaluation
EJ1515368	Rat Malondialdehyde(MDA) ELISA Kit	BioReagent	Rat MDA detection	Used for MDA-related detection in rat acute liver injury models
T1521744	Total Glutathione (T-GSH) Content Assay Kit (DTNB, Micro Method)	BioReagent	Glutathione system	Used for total glutathione detection; suitable for evaluating antioxidant capacity in APAP, CCl4, and ethanol models
T1521745	Total Glutathione (T-GSH) Content Assay Kit (DTNB, Colorimetric Method)	BioReagent	Glutathione system	Used for colorimetric detection of total glutathione content
R1492762	Reduced Glutathione (GSH) Content Assay Kit (DTNB, Micro Method)	BioReagent	GSH content	Used for evaluating GSH depletion and antioxidant capacity, especially in APAP models
R1505409	Reduced Glutathione (GSH) Content Assay Kit (DTNB, Colorimetric Method)	BioReagent	GSH content	Used for colorimetric detection of GSH content
G1505763	Glutathione Peroxidase (GSH-Px) Activity Assay Kit (DTNB, Micro Method)	BioReagent	Antioxidant enzyme activity	Used for detecting GSH-Px activity; suitable for oxidative stress and antioxidant defense evaluation
G1505754	Glutathione Peroxidase (GSH-Px) Activity Assay Kit (DTNB, Colorimetric Method)	BioReagent	Antioxidant enzyme activity	Used for colorimetric detection of GSH-Px activity
T1373303	Total Superoxide Dismutase (SOD) Assay Kit (NBT Riboflavin Microplate Method)	BioReagent	SOD activity	Used for microplate-based total SOD detection; suitable for evaluating hepatic antioxidant capacity
T1373360	Total Superoxide Dismutase (SOD) Assay Kit (NBT Riboflavin Colorimetric Method)	BioReagent	SOD activity	Used for colorimetric total SOD detection
T1505644	Total Superoxide Dismutase (T-SOD) Activity Assay Kit (WST-8, Micro Method)	BioReagent	SOD activity	Used for total SOD activity detection in the WST-8 system
T1521754	Total Superoxide Dismutase (SOD) Activity Assay Kit (Pyrogallol, UV Colorimetric Method)	BioReagent	SOD activity	Used for SOD activity detection in UV colorimetric systems
EJ1512250	Rat Tumor Necrosis Factor Alpha (TNF-α) ELISA Kit	BioReagent	Inflammatory factor	Used for TNF-α detection in rat acute liver injury models
EJ1511734	Mouse Tumor Necrosis Factor Alpha (TNF-α) ELISA Kit	BioReagent	Inflammatory factor	Used for TNF-α detection in mouse acute liver injury models
EJ1513094	Mouse Tumor Necrosis Factor Alpha (TNF-α) ELISA Kit	BioReagent	Inflammatory factor	Used for TNF-α detection in mouse inflammatory liver injury
EJ1512162	Rat Interleukin 6 (IL-6) ELISA Kit	BioReagent	Inflammatory factor	Used for IL-6 detection in rat acute liver injury models
EJ1511733	Mouse Interleukin 6 (IL-6) ELISA Kit	BioReagent	Inflammatory factor	Used for IL-6 detection in mouse acute liver injury models
EJ1512935	Mouse Interleukin 6 (IL-6) ELISA Kit	BioReagent	Inflammatory factor	Used for IL-6 detection in mouse inflammatory liver injury
EJ1515430	Rat Lipopolysaccharide (LPS) ELISA Kit	BioReagent	Endotoxin-related indicator	Used for evaluating endotoxin responses in rat D-GalN/LPS or ethanol-related models
EJ1515540	Mouse Lipopolysaccharides(LPS) ELISA Kit	BioReagent	Endotoxin-related indicator	Used for detecting LPS-related inflammatory responses and endotoxin levels in mice
EJ1512280	Rat Lipopolysaccharide Binding Protein (LBP) ELISA Kit	BioReagent	Endotoxin-binding protein	Used for studies of endotoxin responses, gut-derived LPS translocation, and inflammatory mechanisms in rats
EJ1513133	Mouse Lipopolysaccharide Binding Protein (LBP) ELISA Kit	BioReagent	Endotoxin-binding protein	Used for studies of endotoxin responses and D-GalN/LPS model mechanisms in mice
H1506002	Modified Hematoxylin-Eosin (HE) Staining Kit	BioReagent,for cell culture,for microscopy	Histopathology	Used for observing hepatic necrosis, inflammatory infiltration, and tissue architecture
H1508526	Hematoxylin-Eosin (HE) High-Definition Consistent Staining Kit (High-Definition Stable Staining)	BioReagent,for microscopy,Biological Stain	Histopathology	Used for HE staining and pathological evaluation of liver tissue
H1508460	Hematoxylin-Eosin (HE) Staining Kit (with Differentiating Solution)	BioReagent,for microscopy,Biological Stain	Histopathology	Used for routine HE staining; suitable for pathological analysis of acute liver injury
H1508459	Hematoxylin-Eosin (HE) Staining Kit (with Differentiating Solution and Bluing Solution)	BioReagent,for microscopy,Biological Stain	Histopathology	Used for HE staining and pathological morphology observation of liver tissue
B774558	Bile Pigment Staining Solution (Modified Fouchet Method)	BioReagent, Biological Stain, for microscopy	Bile pigment staining	Used for histological observation of bile pigment deposition, cholestasis, or bilirubin-related changes
B598358	Biotin TUNEL apoptosis Kit		Cell death	Used for detecting apoptosis in liver tissue or cells
T1456509	Colorimetric TUNEL Apoptosis Assay Kit	BioReagent,比色法,for microscopy	Cell death	Used for chromogenic TUNEL detection; suitable for microscopic observation of tissue sections
A598363	Aladdin ® 488 TUNEL apoptosis Kit (green fluorescence)		Cell death	Used for fluorescent TUNEL detection; suitable for localization analysis of apoptotic cells
A598361	Aladdin ® 555 TUNEL apoptosis Kit (orange red fluorescence)		Cell death	Used for fluorescent TUNEL detection and combination with multiplex staining
A598362	Aladdin ® 594 TUNEL apoptosis Kit (red fluorescence)		Cell death	Used for red fluorescent TUNEL detection
A598360	Aladdin ® 640 TUNEL apoptosis Kit (far red fluorescence)		Cell death	Used for far-red fluorescent TUNEL detection; suitable for multicolor immunofluorescence experiments

7 Frequently Asked Questions

7.1 Should CCl4 or APAP be selected for acute liver injury modeling?

CCl4 is more suitable for studying free radical injury, lipid peroxidation, and membrane structure disruption, whereas APAP is more suitable for studying drug-induced liver injury, GSH depletion, and mitochondrial injury. If the experimental objective is to screen antioxidant hepatoprotective agents, the CCl4 model can be prioritized. If the focus is drug metabolic toxicity or detoxification mechanisms, the APAP model is more appropriate.

7.2 What is the difference between the ConA model and the D-GalN/LPS model?

The ConA model is more oriented toward T cell- and NK cell-mediated immune liver injury and is suitable for studying immune hepatitis and T cell-related inflammation. The D-GalN/LPS model is more oriented toward endotoxin-, macrophage-, and TNF-α-mediated injury and is suitable for studying inflammatory factor networks and early mechanisms of acute liver failure.

7.3 Why do results decline after a certain time point in the CCl4 model?

After acute CCl4 injury, the liver has strong self-repair capacity. If sampling is too late, ALT and AST may begin to decrease, and the necrotic area may enter the repair phase, affecting the interpretation of injury severity and pharmacological efficacy.

CCl4 is suitable for oxidative stress and membrane injury studies, APAP is suitable for drug-induced hepatotoxicity studies, ConA and D-GalN/LPS are suitable for immune inflammation-related studies, and ethanol models are suitable for studies of alcohol metabolism, lipid deposition, and the gut-liver axis.

For more related articles, please see below:

[1] The Technology Driving Biomedical Revolution — Animal Modeling

[2] Animal Modeling—Tumor Disease Models

[3] A Detailed Guide to the Construction of Animal Models for Metabolic Diseases

[4] Methods for Establishing Animal Models of Cardiovascular Diseases

[5] Methods for Establishing Models of Nervous System Diseases

[6] Construction of a subcutaneous hormonal tumor model of melanoma