Establishment and Evaluation of Animal Models of Gastric Ulcer: Chemical Induction, Stress Injury, Infection Models, and Healing Studies

Animal models of gastric ulcer are used to simulate gastric mucosal barrier disruption, acid-related injury, inflammatory infiltration, oxidative stress, and ulcer repair processes. Model selection should be centered on the research objective: ethanol- or NSAID-induced models are commonly used for acute mucosal protection studies, acetic acid-induced models are often used for chronic healing studies, pylorus ligation models are suitable for acid secretion mechanisms, and Helicobacter pylori infection models are required for infection-related mechanisms.

Keywords: gastric ulcer model; animal modeling; ethanol induction; NSAIDs; acetic acid ulcer; stress ulcer; Helicobacter pylori; gastric mucosal injury

1 Experimental Positioning of Gastric Ulcer Models

1.1 Core Objectives of Model Establishment

(1) Acute gastric mucosal injury

Acute models mainly focus on gastric mucosal barrier disruption, hemorrhagic erosion, oxidative stress, and increased inflammatory factors. Ethanol, indomethacin, aspirin, and stress stimulation can all induce gastric mucosal injury within a short period, making these models suitable for evaluating the gastric mucosal protective effects of candidate drugs.

(2) Chronic ulcer repair

Chronic models focus more on re-epithelialization at the ulcer margin, granulation tissue formation, angiogenesis, and tissue remodeling. The acetic acid-induced model can form chronic ulcer lesions with relatively stable boundaries and is suitable for studying mechanisms related to EGF, VEGF, collagen deposition, and mucosal repair.

(3) Etiology-related mechanisms

Different models correspond to different pathogenic mechanisms. NSAID models emphasize inhibition of prostaglandin synthesis and reduced mucosal defense; pylorus ligation models highlight the effects of gastric acid and pepsin; ischemia-reperfusion models emphasize oxidative stress and microcirculatory disturbance; Helicobacter pylori infection models are used to analyze infection, inflammation, and chronic mucosal lesions.

1.2 Experimental Animals and Model Selection

Rats and mice are the most commonly used animals for gastric ulcer modeling. Sprague-Dawley and Wistar rats are commonly used for ulcer area measurement, gastric juice analysis, and histological evaluation. Mice are suitable for mechanistic studies, genetically modified models, and infection-related immune analysis. Mongolian gerbils are more sensitive to chronic Helicobacter pylori infection and gastric pathological changes, and can be used for studies of infection-related gastric diseases.

Table 1 Selection Logic for Animal Models of Gastric Ulcer

Research Objective	Recommended Model	Main Mechanism	Applicable Evaluation Indicators
Evaluation of acute mucosal protection	Ethanol-induced model	Mucosal barrier disruption, hemorrhagic injury, oxidative stress	Ulcer index, MDA, SOD, HE staining
NSAID-related gastric injury research	Indomethacin or aspirin model	Decreased prostaglandins, weakened mucus barrier, inflammatory response	PGE2, MPO, TNF-α, IL-6
Chronic ulcer healing mechanisms	Acetic acid-induced model	Local tissue necrosis, chronic inflammation, repair and remodeling	Ulcer area, EGF, VEGF, collagen deposition
Stress ulcer research	Water immersion restraint or cold restraint model	Neuroendocrine stress, reduced mucosal blood flow	Ulcer index, gastric mucosal blood flow, oxidative stress
Acid secretion-related injury	Pylorus ligation model	Accumulation of gastric acid and pepsin	Gastric juice volume, pH, total acidity, pepsin activity
Infection-related ulcer research	Helicobacter pylori infection model	Chronic inflammation, bacterial colonization, epithelial injury	Bacterial load, inflammation score, IL-1β, TNF-α
Microcirculatory disturbance and oxidative injury	Ischemia-reperfusion model	Blood flow obstruction, increased ROS, inflammatory infiltration	MDA, SOD, MPO, tissue necrosis area

2 Chemically Induced Gastric Ulcer Models

2.1 Ethanol-Induced Model

(1) Model mechanism

Ethanol can rapidly disrupt the gastric mucus layer and epithelial barrier, allowing gastric acid, oxidative stress, and inflammatory responses to jointly cause mucosal hemorrhage, necrosis, and erosion. This model mainly presents as acute gastric mucosal injury and is suitable for evaluating antioxidant, anti-inflammatory, and mucosal protective drugs.

(2) Experimental interpretation

In the ethanol model, ulcer area and hemorrhagic bands are relatively intuitive, but the degree of injury is significantly affected by ethanol concentration, administration volume, fasting time, and animal body weight. If the model is used for drug screening, positive control, model control, and pretreatment groups should be included, and oxidative stress and histological indicators should be measured simultaneously.

2.2 NSAID-Induced Model

(1) Model mechanism

NSAIDs such as indomethacin and aspirin can inhibit the cyclooxygenase pathway, reduce prostaglandin production, and weaken gastric mucus secretion, bicarbonate secretion, and mucosal blood flow. This model is more closely related to gastric mucosal injury associated with long-term NSAID use.

(2) Experimental interpretation

In NSAID models, decreased PGE2, increased inflammatory factors, and reduced gastric mucosal defense capacity are important interpretation points. When studying the gastroprotective effects of candidate drugs, ulcer index, PGE2, MPO, TNF-α, IL-6, and gastric mucus content should be observed together to avoid inferring the mechanism solely from ulcer area.

2.3 Acetic Acid-Induced Chronic Ulcer Model

(1) Model mechanism

After local application of acetic acid to the gastric wall, a chronic ulcer lesion with a relatively clear boundary can be formed, followed by inflammatory clearance, granulation tissue formation, angiogenesis, and epithelial repair. This model is more suitable for studying ulcer healing than acute mucosal protection.

(2) Experimental interpretation

Core evaluation indicators in the acetic acid model include reduction in ulcer area, mucosal re-epithelialization, collagen deposition, angiogenesis, and growth factor expression. Changes in EGF, VEGF, TGF-β, COX-2, and tight junction proteins can be used to assess the quality of repair.

Table 2 Comparison of Chemically Induced Gastric Ulcer Models

Model Type	Common Inducer	Main Pathological Features	Advantages	Limitations
Ethanol-induced model	Ethanol	Acute hemorrhage, erosion, mucosal necrosis	Rapid modeling; suitable for screening mucosal protective drugs	Injury is mainly acute, with insufficient chronic repair features
NSAID-induced model	Indomethacin	Decreased prostaglandins, enhanced inflammatory response, impaired mucosal barrier	Close to NSAID-related gastric injury	Sensitive to dose, fasting status, and administration route
NSAID-induced model	Aspirin	Reduced gastric mucosal defense, acid-related injury, and inflammatory response	Suitable for drug-induced gastric mucosal injury research	Model intensity is affected by dose and administration period
Acetic acid chronic model	Acetic acid	Chronic ulcer, marginal repair, granulation tissue formation	Suitable for studying ulcer healing mechanisms	More complex operation and high requirement for consistency of local treatment
Acid injury-related model	Hydrochloric acid	Acidic stimulation, barrier disruption, and local mucosal injury	Can be used to simulate acid-related injury conditions	Still differs from complex ulcer etiologies when used alone

3 Stress-, Infection-, and Surgery-Related Models

3.1 Stress-Induced Gastric Ulcer Models

(1) Water immersion restraint stress model

Water immersion restraint stress causes decreased mucosal blood flow, altered gastric acid secretion, and enhanced oxidative stress through combined activity restriction, cold stimulation, and sympathetic activation. This model is suitable for studying stress ulcers, neuroendocrine regulation, and gastric mucosal microcirculatory injury.

(2) Cold restraint stress model

Cold restraint stress emphasizes the combined stimulation of low temperature and restraint, and is often used to observe gastric mucosal injury under acute stress conditions. Temperature, restraint duration, and animal status should be strictly controlled during experiments to reduce intra-group variation.

3.2 Pylorus Ligation Model

The pylorus ligation model blocks gastric emptying, causing gastric acid and pepsin to accumulate in the stomach and induce acid-related ulcers. This model is suitable for studying gastric acid secretion, pepsin activity, and the effects of antacid drugs. Result evaluation should include gastric juice volume, pH, total acidity, and pepsin activity, not only ulcer area.

3.3 Ischemia-Reperfusion Model

The ischemia-reperfusion model induces oxidative stress, inflammatory cell infiltration, and microcirculatory disturbance through gastric blood flow obstruction followed by reperfusion. This model is suitable for studying ROS, mitochondrial injury, endothelial function, and inflammation-mediated gastric mucosal injury. MDA, SOD, GSH, MPO, and tissue necrosis area are commonly used evaluation indicators.

3.4 Helicobacter pylori Infection Model

The Helicobacter pylori infection model is used to simulate infection-related gastritis, mucosal injury, and ulcer susceptibility. Common strains include H. pylori SS1, and animals may include mice or Mongolian gerbils. This model requires a relatively long period and should be evaluated by bacterial colonization detection, inflammation scoring, histological observation, and inflammatory factor analysis.

Table 3 Comparison of Stress-, Infection-, and Surgery-Related Gastric Ulcer Models

Model Type	Modeling Characteristics	Main Mechanism	Suitable Research Direction	Key Control Points
Water immersion restraint stress model	Restraint combined with water immersion stimulation	Decreased mucosal blood flow and neuroendocrine stress	Stress ulcer and microcirculatory injury	Water temperature, restraint duration, animal status
Cold restraint stress model	Restraint combined with low-temperature stimulation	Sympathetic activation and oxidative stress	Acute stress injury	Temperature and exposure duration
Pylorus ligation model	Surgical blockage of gastric emptying	Accumulation of gastric acid and pepsin	Acid secretion and antacid drug evaluation	Ligation site and postoperative observation time
Ischemia-reperfusion model	Reperfusion after blood flow obstruction	Increased ROS, inflammatory infiltration, microcirculatory disturbance	Oxidative stress and blood flow-related injury	Ischemia duration and reperfusion duration
Helicobacter pylori infection model	Long-term infection after bacterial inoculation	Chronic inflammation, bacterial colonization, epithelial injury	Infection-related gastric disease mechanisms	Bacterial viability, inoculation frequency, infection period

4 Supplementary Applications of In Vitro and Ex Vivo Models

4.1 Gastric Epithelial Cell Injury Models

Gastric epithelial cells such as GES-1 and AGS can be used for studies of H₂O₂-, ethanol-, NSAID-, or inflammation-induced cell injury. Cell models are suitable for preliminary mechanistic screening, including oxidative stress, inflammatory signaling, tight junction protein expression, apoptosis, and the protective effects of candidate drugs.

Cell models cannot fully simulate gastric acid secretion, mucosal blood flow, immune infiltration, and tissue repair processes. Therefore, in vitro results should be used as mechanistic clues, while key conclusions still require validation using animal models or histological evidence.

4.2 Ex Vivo Gastric Tissue Models

Ex vivo gastric tissue or gastric mucosal perfusion models can be used to observe the direct effects of drugs on the gastric mucosal barrier, epithelial integrity, and local injury. This model reduces interference from systemic metabolism and neuroendocrine factors, but tissue viability is limited, making it suitable as a supplementary validation tool for pharmacodynamic and mechanistic studies.

Table 4 Application Positioning of In Vivo and In Vitro Models in Gastric Ulcer Research

Model Level	Common Systems	Applicable Questions	Main Limitations
Animal models	Rats, mice, Mongolian gerbils	Ulcer formation, inflammatory infiltration, tissue repair, pharmacodynamic evaluation	Higher cost; requires ethical approval and control of model consistency
Gastric epithelial cell models	GES-1, AGS	Oxidative stress, apoptosis, barrier proteins, drug mechanism screening	Lack of gastric acid, blood flow, and immune microenvironment
Ex vivo gastric tissue models	Ex vivo gastric mucosa or gastric tissue slices	Local mucosal response and direct drug effects	Short observation window and difficulty simulating long-term repair

5 Evaluation Indicators for Gastric Ulcer Models

5.1 Gross and Histological Evaluation

(1) Ulcer index

The ulcer index is usually calculated based on ulcer area, number, length, or severity of hemorrhagic injury, and is the most intuitive endpoint indicator in gastric ulcer models. In acute models, hemorrhagic bands and erosion area should be evaluated; in chronic models, ulcer area reduction and marginal repair should be emphasized.

(2) Histological evaluation

HE staining can reveal epithelial shedding, mucosal necrosis, inflammatory cell infiltration, and glandular structure disruption. PAS staining can be used to evaluate the gastric mucus layer and glycoprotein protective barrier. In chronic ulcer models, Masson staining can also be used to observe collagen deposition and tissue repair status.

5.2 Biochemical and Molecular Indicators

(1) Gastric acid- and digestive enzyme-related indicators

In pylorus ligation models and acid-related injury studies, gastric juice volume, pH, total acidity, and pepsin activity should be measured. If antacid drugs or gastric acid secretion inhibitors are being evaluated, these indicators have greater mechanistic value than ulcer area alone.

(2) Oxidative stress and inflammatory indicators

MDA, SOD, GSH, GSH-Px, and MPO are commonly used to evaluate oxidative injury, antioxidant defense, and inflammatory infiltration. TNF-α, IL-1β, and IL-6 can be used to analyze gastric mucosal inflammatory responses. Oxidative stress indicators are especially valuable in ethanol, stress, and ischemia-reperfusion models, while inflammatory factors and MPO better reflect the injury process in NSAID- and infection-related models.

(3) Barrier repair and angiogenesis indicators

Occludin, ZO-1, claudins, MUC1, MUC5AC, EGF, VEGF, and TGF-β can be used to evaluate gastric mucosal barrier integrity and repair processes. In chronic ulcer healing studies, these indicators should be interpreted together with histological repair results.

Table 5 Common Evaluation Indicators for Gastric Ulcer Models

Evaluation Level	Common Indicators	Application Value	Applicable Models
Gross injury	Ulcer area, ulcer index, hemorrhagic bands	Determines modeling success and drug protective effects	Ethanol, NSAIDs, stress, pylorus ligation
Histology	HE, PAS, Masson	Evaluates necrosis depth, inflammatory infiltration, mucus layer, and repair status	Acute and chronic models
Gastric acid secretion	Gastric juice volume, pH, total acidity	Evaluates acid-related injury and antacid efficacy	Pylorus ligation model
Digestive enzymes	Pepsin activity, PGⅠ, PGⅡ	Analyzes the gastric acid-pepsin injury axis and gastric functional status	Pylorus ligation and acid-related injury models
Oxidative stress	MDA, SOD, GSH, GSH-Px	Determines ROS-mediated injury and antioxidant effects	Ethanol, stress, ischemia-reperfusion
Inflammatory response	TNF-α, IL-1β, IL-6, MPO	Evaluates inflammatory cell infiltration and cytokine release	NSAIDs, infection, ischemia-reperfusion
Barrier repair	ZO-1, occludin, MUC5AC, EGF, VEGF	Evaluates mucosal barrier and ulcer healing	Acetic acid chronic ulcer and drug repair studies

6 Selection of Related Products and Materials

Table 6-1 Products Related to Oxidative Stress Evaluation

Product Category	Cat. No.	Product/Material Name	Grade & Purity	Application Positioning
Lipid peroxidation detection	M1508248	Malondialdehyde (MDA) Content Assay Kit (TBA, Colorimetric Method)	BioReagent	Used for detecting lipid peroxidation levels in gastric mucosal tissue; suitable for ethanol, stress, and ischemia-reperfusion models
Lipid peroxidation detection	M1508267	Malondialdehyde (MDA) Content Assay Kit (TBA, Fluorometric Method)	BioReagent	Used for low-content samples or higher-sensitivity MDA detection
Lipid oxidation detection	L486287	Lipid Peroxidation (MDA) Assay Kit	Sufficient for 100 colorimetric or fluorometric tests	Used for evaluating lipid oxidative injury in gastric mucosa and can serve as a supplementary MDA detection option
Animal sample MDA detection	EJ1515368	Rat Malondialdehyde(MDA) ELISA Kit	BioReagent	Used for detecting MDA levels in rat gastric ulcer models
SOD activity detection	T1505644	Total Superoxide Dismutase (T-SOD) Activity Assay Kit (WST-8, Micro Method)	BioReagent	Used for detecting SOD activity in gastric mucosal tissue; suitable for small-volume samples and microplate readings
SOD activity detection	T1373303	Total Superoxide Dismutase (SOD) Assay Kit (NBT Riboflavin Microplate Method)	BioReagent	Used for total SOD activity evaluation and oxidative stress mechanism analysis
SOD activity detection	T1521754	Total Superoxide Dismutase (SOD) Activity Assay Kit (Pyrogallol, UV Colorimetric Method)	BioReagent	Used for detecting SOD activity by UV colorimetry
Animal sample SOD detection	EJ1512354	Rat Superoxide Dismutases (SOD) ELISA Kit	BioReagent	Used for detecting SOD levels in rat samples
Animal sample SOD detection	EJ1513267	Mouse Superoxide Dismutases (SOD) ELISA Kit	BioReagent	Used for detecting SOD levels in mouse gastric injury models
Glutathione detection	T1521744	Total Glutathione (T-GSH) Content Assay Kit (DTNB, Micro Method)	BioReagent	Used for evaluating glutathione antioxidant reserves in gastric mucosa
Glutathione detection	R1492762	Reduced Glutathione (GSH) Content Assay Kit (DTNB, Micro Method)	BioReagent	Used for detecting reduced GSH levels and evaluating redox status
GSH-Px activity detection	G1505763	Glutathione Peroxidase (GSH-Px) Activity Assay Kit (DTNB, Micro Method)	BioReagent	Used for evaluating antioxidant enzyme system activity in gastric mucosa

Table 6-2 Products Related to Inflammatory Response Evaluation

Product Category	Cat. No.	Product/Material Name	Grade & Purity	Application Positioning
Neutrophil infiltration detection	M1515794	Myeloperoxidase (MPO) Activity Assay Kit (o-Dianisidine, Micro Method)	BioReagent	Used for evaluating neutrophil infiltration and inflammatory injury in gastric mucosa
Animal sample MPO detection	EJ1512429	Rat Myeloperoxidase (MPO) ELISA Kit	BioReagent	Used for detecting MPO levels in rat gastric ulcer models
Animal sample MPO detection	EJ1513379	Mouse Myeloperoxidase (MPO) ELISA Kit	BioReagent	Used for evaluating inflammatory injury in mouse gastric mucosa
Inflammatory factor detection	EJ1512250	Rat Tumor Necrosis Factor Alpha (TNF-α) ELISA Kit	BioReagent	Used for detecting TNF-α levels in rat gastric ulcer models
Inflammatory factor detection	EJ1511734	Mouse Tumor Necrosis Factor Alpha (TNF-α) ELISA Kit	BioReagent	Used for evaluating TNF-α-mediated inflammatory responses in mouse models
Inflammatory factor detection	EJ1512147	Rat Interleukin 1 Beta (IL-1β) ELISA Kit	BioReagent	Used for detecting inflammatory factors in rat gastric mucosa
Inflammatory factor detection	EJ1511731	Mouse Interleukin 1 Beta (IL-1β) ELISA Kit	BioReagent	Used for detecting IL-1β levels in mouse gastric injury models
Inflammatory factor detection	EJ1512162	Rat Interleukin 6 (IL-6) ELISA Kit	BioReagent	Used for evaluating inflammatory responses in rat gastric ulcers
Inflammatory factor detection	EJ1511733	Mouse Interleukin 6 (IL-6) ELISA Kit	BioReagent	Used for detecting IL-6 in mouse gastric mucosal inflammation models
Human cell model detection	EJ1514669	Human Tumor Necrosis Factor Alpha (TNF-α) ELISA Kit	BioReagent	Used for detecting inflammatory factors in human cell models such as GES-1 and AGS
Human cell model detection	EJ1514350	Human Interleukin 1 Beta (IL-1β) ELISA Kit	BioReagent	Used for analyzing inflammatory responses in human gastric epithelial cells
Human cell model detection	EJ1514388	Human Interleukin 6 (IL-6) ELISA Kit	BioReagent	Used for detecting IL-6 release in human cell injury models

Table 6-3 Products Related to Gastric Acid, Pepsin, and Ulcer Repair

Product Category	Cat. No.	Product/Material Name	Grade & Purity	Application Positioning
Pepsin activity detection	P1521970	Pepsin Activity Assay Kit (Micro Method)	BioReagent	Used for detecting pepsin activity in pylorus ligation models
Pepsin activity detection	P1521971	Pepsin Activity Assay Kit (Colorimetric Method)	BioReagent	Used for evaluating the acid-pepsin injury axis
Gastric function-related detection	EJ1512258	Rat Pepsinogen Ⅰ(PGⅠ) ELISA Kit	BioReagent	Used for evaluating gastric mucosal injury and gastric functional status in rats
Gastric function-related detection	EJ1512259	Rat Pepsinogen Ⅱ(PGⅡ) ELISA Kit	BioReagent	Used for detecting PGⅡ levels in rat models
Gastric function-related detection	EJ1513103	Mouse Pepsinogen Ⅰ(PGⅠ) ELISA Kit	BioReagent	Used for detecting PGⅠ levels in mouse gastric injury models
Gastric function-related detection	EJ1513104	Mouse Pepsinogen Ⅱ(PGⅡ) ELISA Kit	BioReagent	Used for detecting PGⅡ levels in mouse models
Human cell/sample detection	EJ1514694	Human Pepsin (Pepsin) ELISA Kit	BioReagent	Used for pepsin-related detection in human samples or in vitro models
Epithelial repair detection	EJ1512336	Rat Epidermal Growth Factor (EGF) ELISA Kit	BioReagent	Used for analyzing chronic ulcer healing and epithelial repair mechanisms in rats
Epithelial repair detection	EJ1513246	Mouse Epidermal Growth Factor (EGF) ELISA Kit	BioReagent	Used for detecting EGF levels in mouse ulcer repair models
Human cell/sample detection	EJ1514913	Human Epidermal Growth Factor (EGF) ELISA Kit	BioReagent	Used for detecting EGF in human gastric epithelial cells or related samples
Angiogenesis detection	EJ1512307	Rat Vascular Endothelial Growth Factor (VEGF) ELISA Kit	BioReagent	Used for evaluating angiogenesis and chronic ulcer healing in rats
Angiogenesis detection	EJ1513205	Mouse Vascular Endothelial Growth Factor (VEGF) ELISA Kit	BioReagent	Used for detecting VEGF-mediated repair responses in mouse models
Human cell/sample detection	EJ1514854	Human Vascular Endothelial Growth Factor (VEGF) ELISA Kit	BioReagent	Used for detecting VEGF levels in human cells or clinically related samples

7 Frequently Asked Questions

7.1 How should models be selected for acute gastric mucosal protection studies?

Ethanol- or NSAID-induced models should be prioritized for acute gastric mucosal protection studies. The ethanol model is more suitable for evaluating mucosal barrier protection, antioxidant effects, and anti-inflammatory activity. NSAID models are more suitable for studying decreased prostaglandins, weakened mucus barrier, and drug-related gastric injury. If a candidate drug is positioned as an antacid, the pylorus ligation model is more mechanistically matched.

7.2 How should endpoints be set in the acetic acid-induced chronic ulcer model?

The acetic acid model should not be evaluated only by final ulcer area. Multiple healing time points are recommended, combined with ulcer area measurement, HE staining, Masson staining, EGF, VEGF, and tight junction protein detection to evaluate re-epithelialization, angiogenesis, and tissue remodeling quality.

7.3 How should gastric acid indicators and ulcer index be jointly interpreted in the pylorus ligation model?

In the pylorus ligation model, gastric juice volume, pH, total acidity, and pepsin activity should be measured together. If a drug reduces the ulcer index while also decreasing total acidity or pepsin activity, this supports a relationship with inhibition of acid secretion. If ulcer improvement occurs without obvious changes in acidity, mucosal protection, antioxidant effects, or anti-inflammatory mechanisms should be further analyzed.

7.4 How can intra-group variation be controlled in stress ulcer models?

Stress models are highly sensitive to environmental and operational conditions. Water temperature, ambient temperature, restraint intensity, stress duration, animal body weight, and fasting status should all be standardized. Preliminary experiments are recommended before formal studies to determine conditions that produce stable injury without excessively high mortality.

7.5 How should successful establishment of a Helicobacter pylori infection model be determined?

A successful infection model should not be judged only by completion of inoculation. Gastric tissue bacterial colonization detection, rapid urease testing, histological inflammation scoring, and inflammatory factor levels should be combined. If the model is used for drug intervention studies, antibacterial effects, anti-inflammatory effects, and mucosal repair effects should also be distinguished.

Animal models of gastric ulcer should be selected according to acute injury, chronic repair, acid secretion, stress response, or infection mechanisms. Integrated analysis of ulcer index, histology, biochemical indicators, and molecular markers can improve the interpretability of model results and the reliability of pharmacodynamic evaluation.

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