ArticleExperimental and therapeutic medicine2018
Increased expression of tight junction protein occludin is associated with the protective effect of mosapride against aspirin-induced gastric injury.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Rice bran extract ameliorate heavy metal mixture induced hippocampal toxicity via inhibiting oxido-inflammatory damages and modulating Hmox-1/BDNF/Occludin/Aβ40/Aβ42 in rats.Toxicology research · 2025Article
- Review on recent advancements in understanding acetylsalicylic acid-induced gastrointestinal injury: mechanisms, medication, and dosage refinement.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Activating Transcription Factor 3 Protects against Restraint Stress-Induced Gastrointestinal Injury in Mice.Cells · 2021Article
- Overview on the Discovery and Development of Anti-Inflammatory Drugs: Should the Focus Be on Synthesis or Degradation of PGEJournal of inflammation research · 2021Review
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- Blood-brain barrier dysfunction in ischemic stroke: targeting tight junctions and transporters for vascular protection.American journal of physiology. Cell physiology · 2018Review
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mosapride is known to affect gastric motility, however whether mosapride has anti-ulcergenic effects in gastric mucosal injury is unclear. The aim of the present study was to investigate the effects of mosapride on aspirin-induced gastric injuries. GES-1 cells were cultured and divided into 5 groups: Control group, aspirin injury group (treated with 18.2 mmol/l aspirin) and mosapride pretreatment groups (treated with 0.4, 0.5, or 0.6 µmol/l mosapride). Cell proliferation was evaluated via MTT assay and cell apoptosis was investigated via flow cytometry. The expression of occludin was determined by western blot analysis. A total of 40 male Sprague-Dawley rats were randomized into five groups: Control group, aspirin injury group (150 mg/kg) and mosapride pretreatment groups (0.25, 0.50 or 0.75 mg/kg). Gastric mucosal lesions were induced by administering 200 mg/kg aspirin daily for 4 days. Rats in the mosapride groups were pretreated with mosapride 1 h prior to aspirin administration. Histological changes were evaluated under a light microscope and gastric epithelial TJs were observed via transmission electron microscopy. The results revealed that cell apoptosis was significantly increased in the aspirin injury group compared with the control (P<0.05), whereas apoptosis was significantly decreased in the mosapride pretreatment groups compared with the aspirin group (P<0.05). Cell viability was significantly increased in the mosapride pretreatment groups compared with the aspirin injury group (P<0.05), and that of the aspirin injury group was significantly decreased compared with the control group (P<0.05). Compared with the aspirin injury group, occludin expression was significantly increased in the three mosapride pre-treatment groups (all P<0.05). It was also demonstrated that gastric damage was significantly attenuated in the mosapride pretreatment groups compared with the aspirin injury group (P<0.05). Impaired TJ integrity was observed in aspirin injury group, whereas TJs in the mosapride groups were almost intact. In conclusion, the results of the present study suggest that mosapride exerts a gastroprotective action on aspirin-induced gastric mucosal injury at least in part via attenuating cell apoptosis and increasing occludin expression.
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