ArticleInflammopharmacology2024
Combined effect of pantoprazole and mesenchymal stem cells on experimentally induced gastric ulcer: implication of oxidative stress, inflammation and apoptosis pathways.
Article in Inflammopharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 10 citations in OpenAlex.
- Paraprobiotics Derived FromFood science & nutrition · 2026Article
- Manuka honey as a multifunctional therapeutic against Helicobacter pylori: from chemical profiling to in vitro potency and in vivo gastroprotective efficacy.BMC complementary medicine and therapies · 2026Article
- Anthraquinone Derivative Rufigallol Protects Against Ethanol-Induced Gastric Damage via Modulation of PGEAntioxidants (Basel, Switzerland) · 2026Article
- Geltrex-based protocol for the differentiation of rat adipose tissue-derived mesenchymal stem cells into insulin-producing cells: in vitro and in vivo considerations.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The Traditional Chinese Medicine Compound Hezi Qingyou Formula Controls the MAPK Signaling Pathway for Alleviating Gastric Ulcer Induced by Acetic Acid in Rats.Journal of immunology research · 2026Article
- Article
- The efficacy of bone marrow-derived mesenchymal stem cells in restoring limbal stem cell deficiency in rat model.Scientific reports · 2025Article
- The Improvement of Experimentally Induced Gastric Ulcers in Rats by Inhibiting Vascularization Through the Blocking of the TNF-α Type 1 Receptor.Immunity, inflammation and disease · 2025Article
- Pretreatment withNutrients · 2025Article
- Blocking leukotriene receptors improve experimentally induced gastric ulcers in rats by inhibiting inflammation and apoptosis.International journal of immunopathology and pharmacologyArticle
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Gastric ulcer (GU) is one of the most common diseases of the upper gastrointestinal tract that affects millions of people worldwide. This study aimed to investigate the possible alleviating effect of a combined treatment of pantoprazole (PANTO) and adipose tissue-derived mesenchymal stem cells (ADSCs) in comparison with each treatment alone on the healing process of the experimentally induced GU in rats, and to uncover the involved pathways. Rats were divided into five groups: (1) Control, (2) GU, (3) PANTO, (4) ADSCs and (5) ADSCs + PANTO. Markers of oxidative stress, inflammation and apoptosis were assessed. The current data indicated that PANTO-, ADSCs- and ADSCs + PANTO-treated groups showed significant drop (p < 0.05) in serum advanced oxidation protein products (AOPPs) and advanced glycation end products (AGEPs) along with significant elevation (p < 0.05) in serum TAC versus the untreated GU group. Moreover, the treated groups (PANTO, ADSCs and ADSCs + PANTO) displayed significant down-regulation (p < 0.05) in gastric nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), tumor necrosis factor alpha (TNF-α), cyclooxygenase-2 (COX-2), intercellular adhesion molecule-1 (ICAM-1), matrix metallopeptidase 9 (MMP-9) and caspase-3 along with significant up-regulation (p < 0.05) in vascular endothelial growth factor (VEGF) and peroxisome proliferator-activated receptor gamma (PPARγ) genes expression compared to the untreated GU group. Immunohistochemical examination of gastric tissue for transforming growth factor β1 (TGF-β1), epidermal growth factor (EGF) and proliferating cell nuclear antigen (PCNA) showed moderate to mild and weak immune reactions, respectively in the PANTO-, ADSCs- and ADSCs + PANTO-treated rat. Histopathological investigation of gastric tissue revealed moderate to slight histopathological alterations and almost normal histological features of the epithelial cells, gastric mucosal layer, muscularis mucosa and submucosa in PANTO-, ADSCs- and ADSCs + PANTO-treated rats, respectively. Conclusively, the co-treatment with ADSCs and PANTO evidenced sententious physiological protection against GU by suppressing oxidative stress, inhibiting inflammation and reducing apoptosis with consequent acceleration of gastric tissue healing process.
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