Research Article

Therapeutic Efficacy of Pantoprazole on Surgical Gastric Ulcer Healing in a Rabbit Model

Rafid M. Naeem, Alaa A. Ibrahim, Mohammed M. Jassim*, Mohammed R. Abduljaleel

Department of Surgery and Obstetrics, College of Veterinary Medicine, University of Basrah, Basrah, Iraq.

Received | February 01, 2026; Accepted | March 11, 2026; Published | April 24, 2026

*Correspondence | Mohammed M. Jassim, Department of Surgery and Obstetrics, College of Veterinary Medicine, University of Basrah, Basrah- Iraq; Email: [email protected]

Citation | Naeem RM, Ibrahim AA, Jassim MM, Abduljaleel MR (2026). Therapeutic efficacy of pantoprazole on surgical gastric ulcer healing in a rabbit model. Adv. Anim. Vet. Sci., 14(5):895-905.

DOI | https://dx.doi.org/10.17582/journal.aavs/2026/14.5.895.905

ISSN (Online) | 2307-8316

Copyright: 2026 by the authors. Licensee ResearchersLinks Ltd, England, UK.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

Introduction

A gastric ulcer is defined as an injury that penetrates the submucosal layer and is linked to a fibrotic healing process, where scar development with fibrous protein production is more common than wound contraction. The resulting scar is frequently resorbed if the severity and duration of the gastrointestinal insult are reduced. Permanent scar development may arise from a substantial fibrotic reaction in long-term damage (Oncel and Basson, 2022). The gastric ulcer is a mucosal defect that penetrates the muscularis mucosa. However, the terms “gastric ulceration” and “gastroduodenal ulceration” actually refer to a clinical condition characterized by anatomically confined cracks in the surface of the gastrointestinal mucosa, with a likely multifactorial origin that varies from case to case. Because acid pepsin bathes these ulcers, stomach or proximal duodenal ulcers are also known as peptic ulcers (Parrah et al., 2013).

The normal mucosa of the stomach is constantly renewing. Normal cytoprotective systems in the stomach shield the mucosa against autodigestion by digestive enzymes and gastric acid. Epithelial migration without proliferation quickly repairs superficial epithelial damage (Liu et al., 2023). Many gastrointestinal disorders may be caused by increase acid secretion and have negative effect on gastric mucosa lead to gastric ulcers (Ndidi, 2020), these disorders need the inhibition of stomach acid output. Proton Pump Inhibitors (PPIs) are very effective medications used to reduce stomach acid and treat significant erosive and non-erosive gastrointestinal diseases in animals (Yavuz and Arslan, 2017).

Long-term usage of NSAIDs and corticosteroids can be linked to GI ulcers, which are a dangerous side effect of several clinically significant disease conditions in companion animals. As a result, gastro-protectants are frequently given to companion animals. In spite of this, not much is known about these medications in veterinary patients. To further assess, the effectiveness and proper application of gastro-protectants in animals, more veterinary research is required (Henderson and Webster, 2006).

Glucocorticoids have been linked to a higher chance of gastric hemorrhage and enteritis; the exact mechanism, however, is unknown. Theories include decreased mucus production or mucosal cell renewal rate or changes in gastric mucus composition, possibly from disruption of normal gastric protective mechanisms mediated by prostaglandin (Tseng et al., 2015).

The protocols for the treatment of gastric ulcers depend on the underlying cause, severity of the lesions, and the animal’s overall health. Medical treatment of patients with gastric ulceration is preferred if the underlying cause can be corrected or controlled, blood loss is not life threatening, and the ulcer does not appear to be in danger of immediate perforation. The goal of medical treatment is to increase mucosal defense systems and reduce stomach acidity. Patients with stomach ulcers have been treated with histamine (H2)-receptor antagonists, proton pump inhibitors, sucralfate, antacids, misoprostol, and bismuth subsalicylate. Surgical exploration and resection are recommended when medicinal therapy is not an option due to the severity of the ulcer. The animal should receive a mix of medications intended to preserve the stomach mucosa following surgical treatment (Demitrack et al., 2012; Patel et al., 2018; Cornell, 2012).

After PPIs were first used in clinical settings to treat acid-related illnesses, their use increased dramatically and steadily. Today, PPIs are among the most commonly prescribed medications worldwide, with many afflicted patients receiving PPI treatment for several years (Kinoshita et al., 2018).

Omeprazole and Pantoprazole are substituted benzimidazoles that covalently bind the hydrogen ion (H+)-potassium ion (K+) ATPase enzyme, blocking its activity and thereby blocking secretion of hydrogen ions into the gastric lumen. Proton pump inhibitors are absorbed in an alkaline environment; thus, their uptake is within the proximal duodenum. Proton pump inhibitors are metabolized primarily by the hepatic cytochrome P-450 system. Only pantoprazole is accessible as an injectable medication, despite the fact that all proton pump inhibitors may be used orally. To guarantee that peak serum concentration and maximal proton pump secretion activity coincide, these medicines should be given one hour prior to a meal. Near-complete inhibition of gastric acid secretion requires 3 to 5 days of therapy. Concerns with regard to bacterial overgrowth and decreased absorption of specific compounds have been raised when proton pump inhibitors are used for more than 30 days. Currently, these concerns have not been substantiated in the veterinary literature (Aguilera-Castro et al., 2016; Cornell, 2012).

Although a number of PPI-related side effects have been documented, their clinical significance is still unclear since the data presented in that research is insufficiently strong the majority are based on retrospective observational studies, and the stated hazard ratios are low. PPIs should only be given to patients who would have a significant therapeutic benefit, and high-quality prospective studies should continue to look at any negative effects (Kinoshita et al., 2018).

The study’s objective was to investigate histologically how proton pump inhibitors (pantoprazole) affected a surgically induced gastric ulcer in a rabbit model.

Materials and Methods

Animals

Twelve female rabbits, weighing 1.5-2.0 kg, were utilized in the present study. The animals were maintained in separate cages. They had free access to food and water during a seven-day acclimation period. Animals were deprived of food, but had free access to water, for five hours before surgery (Ibrahim, et al., 2025). After induction of gastric ulcers, rabbits were randomly divided into two groups: group one was ulcerated and treated with antibiotics only (control), and group two was treated with antibiotics plus the proton pump inhibitor (pantoprazole) post-gastric ulceration (treated group).

Mucosal ulcer induction: Under general anesthesia induced by a mixture of xylazine and ketamine (Abduljalel et al., 2025), the stomach was exposed from the abdominal cavity through a midline celiotomy (Figures 1, 2). After performing a gastrotomy, a mucosal ulcer (2 mm) was created by using curved Mayo scissors and thumb forceps to excise the gastric mucosa (Figure 3). The stomach wall was closed with Schmieden and Cushing suturing patterns using 3-0 monofilament synthetic suture (polyglyconate) (Figures 4, 5). The abdominal incision was closed with usual manner (Figure 6). Systemic antibiotic was administered for seven consecutive days post operatively (Yamamoto et al., 2017).

 

 

 

 

 

The pharmaceutical product (proton pump inhibitor) used in the experiment to treat gastric ulcers contained pantoprazole (Strides Pharma, India) and was available as a tablet. Each tablet contained 20 mg, which was dissolved in 10 ml normal saline to obtain a concentration of 2 mg/ml of pantoprazole. The animals in the treated group were orally administered 2 ml (4 mg) of pantoprazole for seven consecutive days (Babitha et al., 2009).

Samples of the stomach ulcer were obtained at three different time points after 3, 7, and 15 days when the animals were humanely sacrificed. After being excised and preserved in 10% neutral buffered formalin, these samples were transported to the University of Basrah’s Veterinary College laboratory for histopathological analysis. The histological sections were stained using hematoxylin and eosin stain (Mohsin et al., 2025). In addition, gastric specimens were evaluated using a scoring system that included grades to assess gastric mucosal injury and neutrophil infiltration (Table 1).

 

Table 1: Histolopathological scoring system (Liu et al., 2016).

State of pathology	Score No.
Mucosal injury	0	Intact
	1	The epithelial lamina desquamation
	2	The superficial lamina propria desquamation or 1/3 gastric glands reduction
	3	The middle lamina propria desquamation or 2/3 gastric glands reduction
	4	lower lamina propria desquamation or >2/3 gastric glands reduction, even submucosal exposure
Infiltrations of Leukocytes	0	Absent
	1	2 to10/HPF
	2	11 to 20/HPF
	3	21to 30/HPF
	4	>31/HPF
hemorrhage	0	Absent
	1	<10% of the total area/LPF
	2	11% to 20% of the total area/LPF
	3	21% to 30% of the total area/LPF
	4	> 30%

 

HPF: high power field; LPF: low power field.

 

Results

Clinical examination

On the first day postoperatively, the experimental animals suffered from a loss of appetite and reduced movement. Gradually, they returned to normal on the third and fourth days. However, after a few days, the health status of the animals in the control group began to decline in terms of appetite and movement.

Statistical analysis

The pathological scoring results were presented as mean values ± standard errors. Data were analyzed using the Independent Samples t-test and One-Way ANOVA with multiple comparison tests, employing a statistical software program (SPSS for Windows, version 22, USA). Significant differences were considered acceptable at (P ≤ 0.05) (Liang et al. 2019; Choudhary, 2018).

 

Gross pathological examination

Control group

Three days post-surgery, there was black, marked lesion at the site of the ulcer. On the 7th day, the ulcer was erythematous and edematous, with edema in the surrounding mucosa. On the 15th day, there was an elevated, edematous, white-colored lesion with a diffuse erythematous area in the mucosa around the ulcers (Figure 7, 8 and 9).

Treated group

Three days post-ulceration, the ulcer was erythematous, smaller in diameter, and had an elevated, edematous border. After 7 and 15 days post-surgery, the ulcer had disappeared, with complete epithelialization of the mucosal surface (Figures 10, 11).

 

 

 

 

 

Histopathological examination

Three days post-surgery, the control group showed mild necrosis and mild infiltration of inflammatory cells (Figure 13A, 17). Furthermore, most of the gastric mucosa, including the gastric foveolae, gastric pits, gastric glands, parietal cells, and chief cells, appeared normal and intact. However, the treated group from the same period revealed a severe peptic ulcer characterized by severe necrosis and damage to the gastric mucosa, with signs of congestion and severe infiltration of inflammatory cells (Figures 13B, 16, 17, 18).

Seven days post-surgery, gastric ulcers in the control group showed the following changes: Severe infiltration of inflammatory cells and accumulation of granulation tissue. The infiltrated inflammatory cells include plasma cells and lymphocytes as well as accumulation of fibroblasts. The damage to the majority of the stomach mucosa, including gastric foveolae, gastric pits, gastric glands, parietal cells and chief cells, was noted in the control group 7 days following the onset of stomach ulcers. In addition, significant buildup of fibrous tissue and a massive infiltration of inflammatory cells were observed (Figures 14A, 16, 17). In contrast, the changes in the pantoprazole-treated group became less severe. The severe changes that appeared 3 days after ulcer induction began to fade. Instead of severe necrosis of the gastric mucosa, a focal area of necrosis was observed, with a regenerative area separated from the necrotic area by granulation tissue. Some infiltration of inflammatory cells was noted, and some cystic shaped gastric glands were evident (Figures 14B, 16, 17).

At the 15-day time point after gastric ulcer induction, histological evaluations of the control group showed severe necrosis, thick granulation tissue, and infiltration of inflammatory cells inside the gastric glands and in the sub-epithelial layer. Dilated, cystically-shaped gastric glands were observed, with infiltrated inflammatory cells, mostly lymphocytes, present inside them (Figures 15A, 16, 17). While, the histopathological changes of the treated group after 15 days after ulcer induction showed that the subepithelial mucosa displays cystic dilation of few of the gastric glands, presence of focal area of inflammation, and presence of regenerated gastric glands (Figures 15B, 16, 17).

 

 

 

 

 

 

Discussion

The very acidic luminal contents are shielded from the stomach epithelium by the gastric mucosal barrier. The stomach mucosa’s cellular layers are sealed by tight junctions, which prevent luminal contents from leaking into or around these cells. The surface of the epithelium is covered in a thick, bicarbonate-rich mucous coating. The strong blood flow to this region swiftly eliminates the tiny quantity of stomach acid that diffuses into epithelial cells. Drugs that reduce acid production can preserve injured GI mucosa, but many illnesses and medications have the potential to disturb the delicate balance between the harsh luminal contents and the GI protective barrier (Demitrack et al., 2012).

The aim of the study was to evaluate the effect of pantoprazole (PPI) after surgically inducing a gastric mucosal ulcer, assessed clinically, grossly, and histopathologically.

On the first postoperative day, the experimental animals suffered from loss of appetite and less movement. Gradually, they returned to normal on the third and fourth days. However, the health status of the animals of control group gradually began to decline. These results demonstrate the protective effect of the proton pump inhibitor on the ulcerated gastric mucosa in treated animals and the progression of the unprotected gastric ulcer in the control group. Proton Pump Inhibitors are highly effective medications used to treat significant erosive and non-erosive gastrointestinal problems in animals as well as to control stomach acid. It relieves clinical signs and heals mucosal damage, and it offers better intragastric pH management over a 24-hour period (McQuaid, 2004).

After 3 days post-surgery in control group, macroscopically, there was a black in color, demarcated lesion at the site of the ulcer while in treated group, ulcers were erythematous and less diameter with elevated edematous border. These results demonstrate the gastroprotective action of the PPI in improving gastric wound healing and the migration of mucosal epithelial cells, which helps decrease the ulcer diameter. Omeprazole and pantoprazole usage led to an elevated stomach pH (>3) after just two days of dosing in a recent canine study. Despite having a brief 1.5-hour serum half-life, PPIs prolong acid inhibition because they permanently deactivate the proton pump, and it takes 36 to 96 hours for new H+/K+ ATPase pump molecules to be synthesized (Foushee, 2000).

At the 7th day, control group showed the ulcer was erythematous and edematous with edema in the surrounding mucosa while at the 15thday, there was elevated edematous white in color lesion with diffuse erythematous lesions in the mucosa around the ulcers. However, after 7, and15 days, the ulcer was disappeared with complete epithelialization of the mucosal surface in treated group. This result showed that inflammatory, erosive, and eventually ulcerative lesions may occur when the stomach mucosal barrier is disrupted. Gastroprotectants are used to heal ulcers and prevent mucosal damage because they enhance mucosal protective mechanisms (Henderson and Webster, 2006).

PPIs are helpful in reducing GI ulcer hemorrhage. One important element in the management of bleeding ulcers is elevated intra-gastric pH. By disrupting the coagulation system, fibrinogen polymerization, and platelet aggregation, both HCl and pepsin impair coagulation (Gisbert et al., 2001).

After 3 days post-surgery, the control group showed mild necrosis and mild infiltration of inflammatory cells. Furthermore, most of the gastric mucosa including gastric foveolae, gastric pits, gastric glands, parietal cells and chief cells are normal and intact. While the treated group revealed severe peptic ulcer and characterized by severe necrosis and damage of gastric mucosa with signs of congestion, severe infiltration of the inflammatory cells, ulceration. The tissue repair phases of the wound-healing process can be inhibited by chronic inflammation (a prolonged inflammatory stage); however, acute inflammation appears early in an improved healing phase (Gao et al., 2024). It hypothesized that the control group’s ulcer was immediately covered by a protective clot/crust (the “black” lesion seen grossly), while the PPI group, with higher pH, might have had a more “clean” but exposed ulcer bed that appears more reactive histologically.

These results disagree with those of Peng et al. (2017), who obtained 75 gastric antral mucosa samples from adult patients who had undergone upper gastrointestinal endoscopy and reported gastrointestinal symptoms. Prior to the stomach biopsy, each patient’s history was documented, including smoking, alcohol usage, and the length of time they had been on PPIs. The samples were assessed using histology. They discovered that PPIs reduced neutrophil infiltration of the gastric mucosa, an effect that may be connected to mucosal atrophy.

Seven days after gastric ulcer induction, the control group exhibited the following changes: severe infiltration of inflammatory cells and accumulation of granulation tissue. The infiltrated inflammatory cells include plasma cells and lymphocytes as well as accumulation of fibroblasts. The damage to the majority of the stomach mucosa, including gastric foveolae, gastric pits, gastric glands, parietal cells, and chief cells was noted. In addition, significant buildup of fibrous tissue and a massive infiltration of inflammatory cells were observed. In contrast, the changes in the treatment group became less severe. The severe changes that appeared 3 days after ulcer induction began to fade. Instead of severe necrosis of the gastric mucosa, a focal area of necrosis was observed, with a regenerative area separated from the necrotic area by granulation tissue. Some infiltration of inflammatory cells was noted, and some cystic shaped gastric glands were evident.

Proton-pump inhibitors permanently attach to hydrogen-potassium ATPase molecules, which results in a dose-dependent and long-lasting suppression of stomach acid output. The inhibition lasts long after the medication is removed from the plasma because acid secretion can only start again after fresh hydrogen-potassium ATPase molecules are produced. Proton-pump inhibitors speed up ulcer healing because of this complete and long-lasting inhibition (Simadibrata et al., 2022).

At the 15-day time point after gastric ulcer induction, the control group showed severe necrosis, thick granulation tissue, and infiltration of inflammatory cells inside the gastric glands and in the subepithelial layer, dilated cystic shaped gastric glands were observed with presence of infiltrated inflammatory cells inside mostly lymphocytes. While, the histopathological changes of the treated group showed that the subepithelial mucosa displays cystic dilation of few of the gastric glands, presence of focal area of inflammation, and presence of regenerated gastric glands, these evident come in agree with (Olivarez et al., 2023). They discovered that PPI usage leads to better intragastric pH management, making it more successful in treating and preventing ulcers.

Conclusion

Pantoprazole, a proton pump inhibitor, is a very effective medication used to reduce stomach acid and treat significant gastrointestinal problems in animals. This study suggests that pantoprazole can potentially treat gastric ulcers by successfully providing partial mucosal protection, thereby enhancing epithelial migration and mucosal regeneration.

ACKNOWLEDGEMENT

We want to thank head of department of surgery and obstetric, Dean of Veterinary Medicine and Basrah university’s president for their support in college laboratory.

NOVELTY STATEMENT

This study provides a novel evaluation of Pantoprazole’s therapeutic impact on surgically induced gastric ulcer in a rabbit model, moving beyond traditional chemical-induced ulcer studies. It demonstrates that Pantoprazole actively reduces the gastric mucosal healing time at the surgical site of ulcer induction by suppression of gastric acid secretion and providing the suitable environment for healing. Therefore, it collaborates with gastric ulcers healing. By utilizing a rabbit model, which more closely mirrors human gastric physiology, this research offers original insights into the prophylactic role of PPIs in post-operative gastric recovery.

AUTHOR’S CONTRIBUTION

All authors equally contributed.

Ethical approval

The Animal Care and Use Committee/College of Veterinary Medicine, University of Basrah, Iraq, followed ethical guidelines and all relevant national and international legislation when designing and conducting this study. (Approval number: 119/37/2026).

Generative AI and AI assisted technology statement

The authors declare that no generative AI and AI assisted technology was used in the creation of this manuscript.

Conflict of interest

The authors have declared no conflict of interest

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