ArticleDigestive diseases and sciences2006
Essential role of pepsin in pathogenesis of acid reflux esophagitis in rats.
Article in Digestive diseases and sciences, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 45 citations in OpenAlex.
- Pathogenesis of pepsin-induced gastroesophageal reflux disease with advanced diagnostic tools and therapeutic implications.Frontiers in medicine · 2025Review
- Global Transcriptomic Analysis of Topical Sodium Alginate Protection against Peptic Damage in an In Vitro Model of Treatment-Resistant Gastroesophageal Reflux Disease.International journal of molecular sciences · 2024Article
- Inhaled fosamprenavir for laryngopharyngeal reflux: Toxicology and fluid dynamics modeling.Laryngoscope investigative otolaryngology · 2024Article
- Amprenavir inhibits pepsin-mediated laryngeal epithelial disruption and E-cadherin cleavage in vitro.Laryngoscope investigative otolaryngology · 2023Article
- The Protease Inhibitor Amprenavir Protects against Pepsin-Induced Esophageal Epithelial Barrier Disruption and Cancer-Associated Changes.International journal of molecular sciences · 2023Article
- Pepsin Triggers Neutrophil Migration Across Acid Damaged Lung Epithelium.Scientific reports · 2019Article
- Melatonin in Prevention of the Sequence from Reflux Esophagitis to Barrett's Esophagus and Esophageal Adenocarcinoma: Experimental and Clinical Perspectives.International journal of molecular sciences · 2018Review
- A Comparison of Alkaline Water and Mediterranean Diet vs Proton Pump Inhibition for Treatment of Laryngopharyngeal Reflux.JAMA otolaryngology-- head & neck surgery · 2017Article
- Protective effects of D-002 on experimentally induced gastroesophageal reflux in rats.World journal of gastroenterology · 2014Article
- Animal model of acid-reflux esophagitis: pathogenic roles of acid/pepsin, prostaglandins, and amino acids.BioMed research international · 2014Review
- Orally administered L-arginine and glycine are highly effective against acid reflux esophagitis in rats.Medical science monitor : international medical journal of experimental and clinical research · 2012Article
- Cross-organ sensitization of thoracic spinal neurons receiving noxious cardiac input in rats with gastroesophageal reflux.American journal of physiology. Gastrointestinal and liver physiology · 2010Article
- Characteristic pathological findings and effects of ecabet sodium in rat reflux esophagitis.World journal of gastroenterology · 2009Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pepsin, a protease activated by gastric acid, is a component of the refluxate, yet the role of pepsin in the pathogenesis of reflux esophagitis has not been well studied. In the present study, we examined the effect of pepstatin, a specific inhibitor of pepsin, on acid reflux esophagitis. Acid reflux esophagitis was induced in rats by ligating both the pylorus and the forestomach for 3 or 4 hr. Pepstatin, ecabet Na (the anti-ulcer drug), and L-glutamine were administered intragastrically after the ligation. Pepstatin or ecabet Na, given intragastrically, significantly prevented esophageal lesions, even though they did not affect basal acid secretion in pylorus-ligated rats. Pepstatin significantly inhibited pepsin activity in vivo and in vitro, while ecabet Na inhibited this activity in vitro. By contrast, L-glutamine given intragastrically aggravated the lesions in a dose-dependent manner, but even in the presence of L-glutamine the development of esophageal lesions was totally prevented by coadministration of pepstatin or ecabet Na. L-Glutamine increased the pH of gastric contents to approximately 2.0, the optimal pH for the proteolytic activity of pepsin in vitro. In addition, intragastric administration of exogenous pepsin worsened the severity of esophageal damage. These results suggest that pepstatin is highly effective against acid reflux esophagitis, without influencing acid secretion, while L-glutamine aggravated these lesions by increasing the pepsin activity by shifting the intraluminal pH to the optimal pH range for proteolytic action. It is assumed that pepsin plays a major pathogenic role in the development of acid reflux esophagitis.
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