Comprehensive Insights into Screening Models for the Pharmacological Evaluation of Antiulcer Activity

Abstract

Background: Peptic ulcer is a prevalent gastrointestinal disorder that develops when the protective mechanisms of the stomach are disrupted in relation to aggressive factors such as gastric acid and pepsin. Contributing risk factors include poor dietary habits, alcohol intake, cigarette smoking, long-term administration of nonsteroidal anti-inflammatory drugs (NSAIDs), and lack of physical activity. The resulting imbalance can cause ulcerative lesions in the stomach, duodenum, or, less commonly, the esophagus. Clinically, patients often present with epigastric discomfort, hematemesis with a coffee-ground appearance, dark tarry stools (melena), and persistent abdominal pain, which typically intensifies following meals and frequently leads them to seek medical consultation. Objective: Multiple experimental models are available to evaluate the antiulcer potential of drug molecules. This review aims to identify the most effective models for the pharmacological assessment of antiulcer activity. Methods: A comprehensive literature search was carried out using various databases with keywords such as “anti-ulcer activity,” “in-vitro models,” and “in-vivo models.” Relevant filters were applied to retrieve the most suitable articles for this review. Results: Numerous research and review articles describe diverse screening models for assessing antiulcer activity in novel drug candidates. Conclusion: Based on the analysis, both in-vitro and in-vivo models have unique advantages. A combined approach utilizing both methods may provide the most reliable and clinically relevant outcomes in antiulcer research. Keywords: anti-ulcer activity, in-vitro models, in-vivo models

Keywords

Introduction

Peptic ulcers (PU) are mucosal defects in the gastrointestinal tract that extend into the muscularis mucosae and are commonly associated with inflammation, oxidative stress, neutrophil accumulation, and necrosis at varying stages [1]. Historically, PU has been one of the most widespread gastrointestinal conditions, affecting millions of individuals across the globe. It is estimated that more than 5–10% of the global population experiences this disorder at some point [2]. Ulceration arises due to disruption of the protective mucosal lining in the stomach, duodenum, or esophagus, which may be linked to inadequate resistance of the gastric mucosa [3].Gastrointestinal diseases, including PU, are among the most common and serious health concerns, as they significantly contribute to pain, morbidity, and reduced quality of life. Reports suggest that 10–15% of the population is affected at any given time. Peptic ulcer disease (PUD) is defined by the presence of mucosal breaks in the lining of the stomach, duodenum (the initial segment of the small intestine), or esophagus (food pipe). The pathogenesis involves an imbalance between aggressive elements such as gastric acid, pepsin, Helicobacter pylori infection, and prolonged NSAID use, and protective mechanisms including bicarbonate, mucin, prostaglandins, nitric oxide, peptides, and growth factors. Based on location, ulcers are classified as gastric ulcers when occurring in the stomach and duodenal ulcers when located in the duodenum [4].Clinically, patients may present with epigastric pain that often worsens after meals, vomiting with a coffee-ground appearance, hematochezia, or passage of tarry stools. Eating may aggravate the pain, leading to a burning sensation in the epigastric region. Poor sleep and irregular food habits have also been linked to duodenal ulcer risk. In cases where symptoms are unresponsive to over-the-counter medications, referral to a gastroenterologist is warranted [5].
From an anatomical perspective, duodenal ulcers most often develop in the duodenal bulb, the region most exposed to gastric acid, while gastric ulcers are usually found along the lesser curvature of the stomach. Earlier theories attributed all upper gastrointestinal ulcers solely to the corrosive actions of gastric acid and pepsin. However, recent findings emphasize the role of H. pylori infection and chronic use of NSAIDs and aspirin in the etiology of PUD [1,6].Globally, PU prevalence is estimated at 200–250 cases per 100,000 population, with a higher incidence reported in developing nations [7]. The pathogenesis is characterized by an imbalance between diminished protective factors such as bicarbonate secretion, prostaglandins (PGs), nitric oxide (NO), and antioxidant defenses, and enhanced aggressive factors such as free radicals, excessive gastric acid output, and pepsin activity [8]. 
Pathogenesis of Peptic Ulcer:
The precise mechanism by which Helicobacter pylori contributes to gastric mucosal damage remains unclear. Depending on the ulcer type, infection with H. pylori may lead to either hypochlorhydria or hyperchlorhydria. Key mediators involved are cytokines that suppress parietal cell activity; however, H. pylori can also exert direct effects by altering the H+/K+ ATPase α-subunit, stimulating calcitonin gene-related peptide (CGRP) sensory neurons associated with somatostatin release, or by reducing gastrin secretion [9]. While gastric ulcer formation is typically linked to reduced acid output, about 10–15% of infected individuals exhibit elevated gastric secretion, largely due to hypergastrinemia combined with diminished antral somatostatin levels [10]. This cascade enhances histamine release from parietal and gastric cells, thereby promoting increased secretion of acid and pepsin. Importantly, eradication of H. pylori has been shown to decrease gastrin mRNA expression while simultaneously elevating somatostatin mRNA expression [11]. 
  
 
  
Fig no-01-Pathogenesis of Peptic Ulcer
 
The principal mechanism underlying NSAID-induced gastroduodenal injury is the systemic inhibition of constitutively expressed cyclooxygenase-1 (COX-1), the enzyme responsible for prostaglandin synthesis. This suppression reduces mucosal blood flow, decreases mucus and bicarbonate secretion, and inhibits epithelial cell turnover. NSAIDs inhibit COX-1 in a reversible and concentration-dependent manner. The use of COX-2–selective NSAIDs in combination with exogenous prostaglandins has been shown to reduce mucosal injury and ulcer risk [12].
Nonetheless, differences in the physicochemical properties of NSAIDs contribute to variability in their toxicity. They compromise mucosal defense by disrupting mucus phospholipids and uncoupling mitochondrial oxidative phosphorylation. In the acidic gastric environment (pH 2), NSAIDs become protonated and can diffuse across lipid membranes into epithelial cells (pH 7.4). Once inside, they ionize and release protons, leading to intracellular trapping. This process disrupts oxidative phosphorylation, decreases ATP generation, increases membrane permeability, and compromises epithelial integrity [13].
The acid secreted under these conditions plays a key role in the pathogenesis of mucosal damage, contributing to duodenal and esophageal injury. Acid secretion is regulated by three pathways—endocrine, paracrine, and neurocrine—that collectively modulate the activity of the approximately one billion parietal cells responsible for hydrogen ion secretion into the gastric lumen. Acetylcholine, released from vagal postganglionic neurons, acts via M3 muscarinic receptors on parietal cells to stimulate acid secretion. Histamine, functioning as a paracrine mediator, binds to H2 receptors on parietal cells, activating adenylate cyclase and increasing intracellular cAMP levels, which enhance acid production [14]. In the endocrine pathway, gastrin released from antral G-cells directly stimulates parietal cells or indirectly enhances acid output by inducing histamine release from enterochromaffin-like cells in the corpus and fundus. Figure 1 summarizes the pathophysiological processes involved in peptic ulcer formation [15].
 
 
 

 
Symptoms and Clinical features of Peptic Ulcer: 
Commercial Treatments for Peptic Ulcer:[16]
 
 

 
Drug Class / Purpose    Common Examples (Generic / Brand)    Notes
Proton Pump Inhibitors (PPIs)    Omeprazole; Pantoprazole (Protonix); Lansoprazole; Rabeprazole; Esomeprazole; Dexlansoprazole    Potent acid suppression; cornerstone of ulcer healing [17]
H?-Receptor Antagonists (H?RAs)    Ranitidine*; Famotidine (Pepcid); Cimetidine; Nizatidine (Axid/Tazac)    Reduce gastric acid; Famotidine also helps in H. pylori regimens[19]
Antacids    Aluminum hydroxide + Magnesium hydroxide (e.g., generic formulations)    Provide rapid neutralization of acid, symptomatic relief [20]
Antibiotics & Combo Regimens    Amoxicillin; Clarithromycin; Metronidazole; Tetracycline; Triple or Quadruple therapy regimens    Used for H. pylori eradication—with PPI and sometimes bismuth[21]
Mucosal Protective Agents & Prostaglandins    Sucralfate; Misoprostol; Rebamipide; Carbenoxolone; Troxipide; Bismuth subsalicylate / subcitrate    Protect gastric lining and promote healing[22]
Anticholinergic/Anxiolytic Combo    Chlordiazepoxide + Clidinium bromide (Librax)    Relieves spasms and abdominal discomfort by reducing acid and calming effects[22]
Table 1 lists of the phytochemical components that were reported to have been extracted from the list of plants used in folk medicine to treat peptic ulcer illness.
 
Plant Name (Abbreviation)    Family    Part Used    Major Phytochemical Constituents    References
Chromolaena odorata (C. odorata)    Asteraceae    Leaves    Alkaloids, flavonoids, tannins, steroids, terpenoids, cardiac glycosides    [18,19]
Alchornea cordifolia (A. cordifolia)    Euphorbiaceae    Leaves    Tannins, terpenoids, glycosides, alkaloids, saponins, flavonoids    [20]
Blighia sapida (B. sapida)    Sapindaceae    Leaves / Stem bark    Cardiac glycosides, saponins, anthraquinones, flavonoids, alkaloids, phlobatannins, terpenes    [21–23]
Cyperus rotundus (C. rotundus)    Cyperaceae    Whole plant    Tannins, alkaloids, triterpenoids, flavonoids, phenolics, saponins, proteins, essential oils, starch, carbohydrates, cardiac glycosides    [24–26]
Azadirachta indica (A. indica)    Meliaceae    Leaves    Alkaloids, saponins, tannins, flavonoids    [27–29]
Calotropis procera (C. procera)    Apocynaceae    Leaves    Flavonoids, polyphenolics, stigmasterol, β-sitosterol, alkaloids, saponins, tannins    [30–32]
Hoslundia opposita (H. opposita)    Lamiaceae    Leaves and roots    Alkaloids, tannins, flavonoids, phenols, terpenoids, saponins, quinones (aqueous and ethanolic extracts)    [33–35]
Kigelia africana (K. africana)    Bignoniaceae    Leaves    Reducing sugars, saponins, flavonoids, alkaloids, phytosterols, coumarins, naphthoquinones, glycosides    [36–38]
Spathodea campanulata (S. campanulata)    Bignoniaceae    Stem bark    Saponins, tannins, anthraquinone glycosides, phenols, carbohydrates, flavonoids, sterols, triterpenoids    [39–42]
Mangifera indica (M. indica)    Anacardiaceae    Leaves    Vitamins, carotenoids, polyphenols, sterols, amino acids, flavonoids, terpenes    [43,44]
Paullinia pinnata (P. pinnata)    Sapindaceae    All parts    Flavonoids, alkaloids, cardiac glycosides, saponins, tannins, carbohydrates, sterols, triterpenoids, steroidal glycosides    [45–49]
Strophanthus hispidus (S. hispidus)    Apocynaceae    Roots    Tannins, glycosides, saponins, flavonoids, alkaloids, resin, rhamnose sugar    [50–52]
Zingiber officinale (Ginger)    Zingiberaceae    Rhizome    Alkaloids, steroids, terpenoids, flavonoids, fats and oils, resins, carbohydrates    [53–58]
 
Models for Antiulcer Activity:
After an extensive review of the available literature, it is evident that numerous experimental models for evaluating antiulcer activity have been developed. Some of these models are now less frequently employed due to methodological limitations or poor reproducibility, while others continue to provide reliable and rapid results. Broadly, these models can be classified into two categories: those performed under controlled laboratory conditions using chemicals and instruments (in vitro), and those requiring the use of live animals (in vivo).
 
  
Chart no 01 In Vitro Antiulcer activity Methods
 

 
 
Chart no 02 In Vivo Antiulcer activity Methods
 
Table no 03 In Vitro Antiulcer Activity Methods
 
Model    Principle / Basis    Key Features / Applications    References
H?/K? ATPase (Proton Pump) Inhibition Assay    Measures the ability of test compounds to inhibit gastric proton pump enzyme (similar to PPIs like omeprazole).    Indicates antisecretory effect by blocking acid secretion at the cellular level.    [59–64]
Urease Inhibition Assay    Targets Helicobacter pylori urease enzyme, responsible for neutralizing gastric acid and aiding bacterial survival.    Helps screen anti-H. pylori and anti-ulcer activity.    [65–70]
Helicobacter pylori Growth Inhibition Assay    Direct assessment of antibacterial effect of compounds against H. pylori cultures.    Useful for plants/extracts with antimicrobial potential.    [71–77]
Cell Line–Based Cytoprotection Models    Gastric epithelial cell lines (e.g., AGS, MKN-28, RGM-1) exposed to ethanol, acid, or NSAIDs. Protective effect of test compound is evaluated.    Mimics gastric mucosal injury in vitro; assesses cytoprotective action.    [78–83]
Mucin Secretion Assay    Assesses ability of compounds to increase or preserve gastric mucus secretion using isolated gastric cells/tissues.    Indicates cytoprotective effect via mucus barrier enhancement.    [84–88]
Lipid Peroxidation / Antioxidant Assay (TBARS, DPPH, etc.)    Oxidative stress is a major factor in ulcerogenesis. Assesses antioxidant potential of extracts (in gastric homogenates or cell lines).    Antioxidant protection correlates with anti-ulcer effect.    [89–91]
Albumin Denaturation / Proteinase Inhibition Assay    Denaturation of proteins contributes to ulcer formation. Agents that prevent protein denaturation or inhibit proteases are protective.    Rapid, simple in-vitro screening model.    [92–95]
Heat-Induced Hemolysis Assay (Anti-inflammatory related)    Evaluates membrane-stabilizing activity of compounds on RBCs. Stable membranes resist ulcerogenic agents.    Indirect marker of ulcer protection.    [96–99]

 
Procedure of In Vitro Antiulcer activity:
1. H?/K?-ATPase Inhibition Assay
Preparation of H?/K?-ATPase Enzyme:
Fresh goat stomach obtained from a local slaughterhouse was used for enzyme preparation. The fundic region was dissected, opened, and the mucosal layer containing parietal cells was carefully scraped. The isolated parietal cells were homogenized in 16 mM Tris buffer (pH 7.4) containing 10% Triton X-100, followed by centrifugation at 6000 rpm for 10 minutes. The resulting supernatant served as the source of H?/K?-ATPase. Protein content in the preparation was quantified using Bradford’s method with BSA as the standard.
Evaluation of Enzyme Inhibition:
For the assay, reaction mixtures containing 0.1 ml of enzyme extract (300 µg) and varying concentrations of plant extract (20–100 µg) were pre-incubated at 37 °C for 60 minutes. The reaction was initiated by adding 2 mM ATP (200 µL), 2 mM MgCl? (200 µL), and 10 mM KCl (200 µL). After 30 minutes of incubation at 37 °C, the reaction was terminated with 4.5% ammonium molybdate, followed by the addition of 60% perchloric acid. The mixture was centrifuged at 2000 rpm for 10 minutes, and the released inorganic phosphate (Pi) was quantified spectrophotometrically at 660 nm using the Fiske–Subbarow method.
For measurement, 1 ml of the supernatant was mixed with 4 ml of Millipore water and 1 ml of 2.5% ammonium molybdate solution, followed by 0.4 ml of ANSA reagent. Absorbance was recorded at 660 nm after 10 minutes at room temperature.
Calculation of Enzyme Activity:
The enzyme activity was expressed as micromoles of Pi released per hour. The percentage inhibition was determined using the formula:
%Inhibition=Activity (control)Activity (control)−Activity (test)×100
The results were presented as Mean ± SEM, showing approximately 16% enzyme inhibition [59–64].
2. Acid Neutralizing Capacity:
Acid-Neutralizing Capacity (ANC) Assay
To determine the acid-neutralizing capacity, 5 mL of the test sample was diluted with distilled water to a final volume of 70 mL. Subsequently, 30 mL of 1N hydrochloric acid was added, and the mixture was stirred continuously for 15 minutes. A few drops of phenolphthalein indicator were then introduced, and the excess (unneutralized) acid was back-titrated against 0.5N sodium hydroxide until a stable pink endpoint was observed. The volume of NaOH consumed was recorded, and ANC was calculated by comparing with a standard antacid formulation.
The acid-neutralizing capacity was expressed in milliequivalents (mEq) using the following equation:
Total mEq=(30×NHCl)−(VNaOH×NNaOH)
where NHClN_{HCl}NHCl and NNaOHN_{NaOH}NNaOH represent the normalities of HCl and NaOH, respectively, and VNaOHV_{NaOH}VNaOH is the volume of NaOH required for the back titration [100,101].
3. Urease Inhibition Assay:
Urease inhibition, an important antiulcer screening method particularly relevant to Helicobacter pylori–associated gastric pathology, was carried out by incubating the test extract with urease (either jack bean urease or H. pylori urease) in phosphate buffer (≈50 mM, pH 7.0) at 37 °C. The enzymatic reaction was initiated by the addition of urea (≈25–50 mM) and allowed to proceed for 15–30 minutes. The amount of ammonia released as a result of urea hydrolysis was determined colorimetrically using the salicylate–hypochlorite (indophenol) method, and absorbance was measured at 630–700 nm.Absorbance from a reagent blank (no enzyme) and a sample blank (sample without enzyme) was subtracted, and inhibition was referenced to an enzyme control lacking inhibitor; a known urease inhibitor (e.g., thiourea or acetohydroxamic acid) served as a positive control. [65–70]
Percentage inhibition was calculated as:
% Inhibition = [1 − ((A_test − A_sample blank) / (A_control − A_reagent blank))] × 100
and potency was expressed as IC?? where appropriate, supporting claims of antiulcer potential via suppression of urease-driven ammonia production and mucosal injury. The percentage of inhibition was determined using the following expression:
4. Helicobacter pylori Growth Inhibition Assay:
The growth inhibitory potential against H. pylori can be determined using either microdilution or agar-based techniques under microaerophilic conditions [102]. In the broth microdilution method, standardized bacterial suspensions (≈10? CFU/mL) are inoculated into Brucella broth or brain–heart infusion medium enriched with serum and selective antibiotics, together with serial dilutions of the test sample [103]. The cultures are incubated at 37 °C for 48–72 hours in a controlled gaseous environment (about 5% O?, 10% CO?, and 85% N?). After incubation, bacterial growth can be quantified spectrophotometrically at 600 nm or by viable colony counts on selective agar plates [104]. The minimum inhibitory concentration (MIC) is defined as the lowest concentration of the test material that completely prevents visible growth when compared to the untreated control [105].As an alternative, agar well diffusion and disk diffusion methods may be employed for preliminary screening. In these assays, the inhibition zones surrounding wells or disks impregnated with the test compound are measured after incubation [106]. For validation purposes, standard antibiotics such as clarithromycin and metronidazole are generally used as positive controls [107].
 

Table no.04 In Vivo Antiulcer activity models 
Model    Principle / Induction Method    Significance / Applications    References
Pylorus Ligation Model (Shay Rat Model)    Ligation of the pyloric region of the stomach leads to the accumulation of gastric secretions, which subsequently results in autodigestion and the development of ulcers.    Used to study antisecretory & cytoprotective effects; evaluates gastric volume, acidity, and ulcer index.    [102–107]
Ethanol/Absolute Alcohol-Induced Ulcer    Ethanol causes direct necrotizing injury to gastric mucosa and reduces mucus production.    Rapid model for screening cytoprotective activity.    
[108–110]

NSAID/Indomethacin-Induced Ulcer    NSAIDs inhibit COX → ↓ prostaglandins → ↓ mucosal defense → ulcer formation.    Mimics clinical NSAID-induced ulcers; useful for prostaglandin-dependent cytoprotective studies.    [111–113]
Stress-Induced Ulcer (Cold Restraint Stress Model)    Restraining and exposing rats to cold leads to vagal stimulation, ischemia, ↑ acid secretion → ulceration.    Mimics stress-related ulcer pathology in humans.    [114–116]
Acetic Acid-Induced Chronic Ulcer    Serosal application of acetic acid on rat stomach produces chronic ulcers with fibrosis.    Useful for evaluating ulcer healing and chronic anti-ulcer activity.    [122–125]
 
1.Pylorous ligation Method:
Scientists utilize pylorus ligation as a recognized experimental technique, which causes stomach ulcers in rats because it allows gastric secretions to build up and create erosion, followed by ulcer formation. The research involved Wistar albino rats, which weighed between 150 and 200 grams. Prior to the procedure, the animals received 24 hours of fasting while they could drink water freely.[117]The animals were randomly allocated into six experimental groups, with each group consisting of six subjects (n = 6).The rats in group I functioned as the negative control because they received 0.5% DMSO through oral administration.  Group II rats served as the standard group and received omeprazole (20 mg/kg, intraperitoneally) [118]. Groups III and IV were administered plant extracts. All treatments were given 60 minutes prior to pylorus ligation, under light ether anesthesia. To avoid coprophagy and inter-animal interference, each rat was housed separately. A midline abdominal incision (approximately 1 inch) was made just below the xiphoid process, and the pyloric end of the stomach was carefully exposed without causing injury. The pylorus was ligated while maintaining its blood supply, after which the stomach was repositioned into the abdominal cavity and the incision closed with sutures. Four hours post-surgery, the animals were sacrificed, and the stomachs were excised and collected in labeled centrifuge tubes [119,120].The gastric juice pH was recorded, and samples were centrifuged to separate the supernatant. Free and total acidity were determined by titration with 0.1 N NaOH. Subsequently, the stomachs were opened along the greater curvature, pinned on cork boards, and examined for ulceration under a binocular microscope [121]. The ulcer index was determined through direct visual assessment of the gastric mucosa.

2.Ethanol Induced Ulceration:
Gastric ulcers were induced by oral administration of 96% ethanol (5 mL/kg). One hour later, the animals were anesthetized using intraperitoneal ketamine (50 mg/kg) combined with xylazine (10 mg/kg). Following dissection, the stomachs were excised and opened along the greater curvature to evaluate the extent and severity of gastric lesions. A portion of the stomach tissue was then homogenized in ice-cold potassium phosphate buffer (0.05 M, pH 7.4) and centrifuged at 5000 rpm for 10 minutes. The resulting supernatant was stored at −80 °C for subsequent estimation of nitric oxide and malondialdehyde levels [108–110]. 
3. Indomethacin Induced Ulceration:
The acetic acid–induced ulcer model is a widely recognized method for evaluating the ulcer-healing efficacy of potential therapeutic agents. In this model, healthy rats are fasted for 24 hours while retaining free access to water. Following anesthesia, a small incision is made in the abdominal wall to expose the stomach. A glass or plastic cylinder (6–8 mm in diameter) is placed on the serosal surface, into which a fixed volume of glacial acetic acid (about 0.05–0.06 mL of an 80% solution) is carefully instilled for roughly 60 seconds to induce a localized necrotic lesion. The acid is then withdrawn, and the affected site is rinsed with saline to prevent additional injury before the abdomen is sutured. After surgery, animals are housed under standard conditions and administered either the test extract, standard drug, or vehicle daily. At the conclusion of the treatment period, rats are sacrificed, and their stomachs are removed, opened along the greater curvature, and examined for ulcer healing. The ulcer index is calculated according to lesion size and severity, and the percentage protection or healing is determined relative to the control group [122–125].
4.Stress Induced Ulceration:
In this model, adult rats are first acclimatized and then deprived of food for about 24 hours, although water is provided freely. The animals are grouped as control, standard, and test, with each group receiving the appropriate treatment such as vehicle, a reference antiulcer drug, or the test sample, administered orally before stress induction. Ulceration is produced by subjecting the rats to combined restraint and cold stress. For this purpose, the animals are gently immobilized in restraining cages and exposed to a low-temperature environment, usually maintained at 4–6 °C, for a period of 2–3 hours. This procedure produces intense physiological stress that leads to gastric mucosal injury and ulcer formation. At the end of the stress exposure, the animals are sacrificed under anesthesia, and their stomachs are excised, opened along the greater curvature, and rinsed with saline to remove gastric contents. The gastric mucosa is then examined for visible lesions, which are scored based on their number and severity to determine the ulcer index. The protective effect of the test sample is assessed by comparing the ulcer index of treated groups with that of the control group, and the percentage inhibition of ulceration is calculated.[114–116]
5. Acetic acid Induced ulcer:
The acetic acid–induced ulcer model is widely employed for evaluating the healing potential of antiulcer agents. In this method, healthy rats are first fasted for 24 hours with free access to water. After anesthetizing the animals, a small incision is made in the abdominal wall to expose the stomach. A glass or plastic cylinder (usually 6–8 mm in diameter) is then placed on the serosal surface of the stomach, and a fixed volume of glacial acetic acid (generally 0.05–0.06 mL of 80% solution) is carefully instilled inside the cylinder for about 60 seconds to produce a localized necrotic lesion. The acid is then aspirated, and the treated area is rinsed thoroughly with saline to prevent further damage before the abdomen is sutured. Following recovery, the animals are housed under standard conditions and receive test compounds, standard drugs, or vehicle for several consecutive days. After the treatment period, the rats are sacrificed, and their stomachs are excised, opened along the greater curvature, and examined for ulcer healing. The ulcer index is calculated based on the size and severity of the lesions, and the percentage protection or healing is determined by comparing treated groups with controls.[122–125]
CONCLUSION:
Peptic ulcer remains a significant gastrointestinal condition influenced by lifestyle choices as well as drug-related factors. To explore and assess new therapeutic options, experimental models play a crucial role. In-vitro models serve as rapid, cost-effective, and well-controlled systems for preliminary evaluation, helping to identify potential candidate compounds. On the other hand, in-vivo models replicate the complex physiological and pathological processes involved in ulcer formation, providing deeper understanding of mechanisms, treatment efficacy, and safety. As both models have distinct advantages and limitations, employing them in combination offers a more thorough, reliable, and clinically meaningful approach to antiulcer research, ultimately aiding in the development of effective therapeutic strategies.
ACKNOWLEDGEMENT:
I would like to express my gratitude to the Department of Science and Technology for providing the research facility at the School of Pharmacy under DST-FIST, which I utilized for my project.
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