Pepsins and the Mucus Barrier in Peptic Ulcer Disease

Allen, Adrian; Pearson, Jeffrey P.; Blackburn, Adrian; Coan, R.; Hutton, David A.; Mall, Anwar Suleman

doi:10.3109/00365528809099130

Cited by 24 publications

(14 citation statements)

References 33 publications

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“…Acid and pepsin are natural aggressors that secreted into the gastric lumen. Pepsin has mucolytic activity and strongly digests the adherent mucus layer at its luminal surface . Pepsin secretion was only stimulated when acid was present.…”

Section: Discussionmentioning

confidence: 99%

Modulation of gastric acid secretion by cannabinoids in rats

Salama

Abdelsalam

Abdel-Salam

et al. 2018

J Biochem & Molecular Tox

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The current study aimed to evaluate the role of cannabinoid receptors in the regulation of gastric acid secretion and oxidative stress in gastric mucosa. To fulfill this aim, gastric acid secretion stimulated with histamine (5 mg/kg, subcutaneous [SC]), 2‐deoxy‐ d‐glucose (D‐G) (200 mg/kg, intravenous) or ‐carbachol (4 μg/kg, SC) in the 4‐hour pylorus‐ligated rats. The CB1R agonist ( N‐arachidonoyl dopamine, 1 mg/kg, SC) inhibited gastric acid secretion stimulated by D‐G and carbachol but not in histamine, reduced pepsin content, and increased mucin secretion. Furthermore, it decreased malondialdehyde (MDA) and nitric oxide (NO) contents with an increase in glutathione (GSH) and paraoxonase 1 (PON‐1). Meanwhile, CB2R antagonist (AM630, 1 mg/kg, SC) inhibited gastric acid secretion stimulated by D‐G and reduced MDA and NO contents with an increase in GSH and PON‐1. Meanwhile, CB1R antagonist rimonabant or CB2R agonist GW 405833 had no effect on stimulated gastric acid secretion. Therefore, both CB1R agonist and CB2R antagonist may exert antisecretory and antioxidant potential in the stomach.

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Section: Discussionmentioning

confidence: 99%

Modulation of gastric acid secretion by cannabinoids in rats

Salama

Abdelsalam

Abdel-Salam

et al. 2018

J Biochem & Molecular Tox

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“…The physiological role of gastric mucus in mucosal protection and ulcer healing has been well established. The polymeric structure of mucus gel becomes weaker and more easily digested during gastric ulceration (1,5). Increased mucus and bicarbonate secretion at the site of injury provides a neutral pH environment that facilities epithelial restitution (30).…”

Section: Discussionmentioning

confidence: 99%

Reduction of EGF is associated with the delay of ulcer healing by cigarette smoking

Ma¹,

Wang²,

Chow³

et al. 2000

American Journal of Physiology-Gastrointestinal and Liver Physi

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Cigarette smoking is associated with peptic ulcer diseases. Smokers have lower levels of salivary epidermal growth factor (EGF) than nonsmokers. We investigated whether reduction of EGF is involved in the delay of gastric ulcer healing by cigarette smoking. Rats with acetic acid-induced ulcers were exposed to cigarette smoke (0, 2, or 4% vol/vol) 1 day after ulcer induction. EGF level was elevated 1 day after ulcer induction in salivary glands and serum, and 4 days after ulcer induction in the gastric mucosa. However, cigarette smoke depressed these beneficial effects and EGF mRNA expression in salivary glands and gastric mucosa. Cigarette smoke delayed gastric ulcer healing and reduced cell proliferation, angiogenesis, and mucus synthesis. Exogenous EGF (10 and 20 microg/kg i.v.) before smoke exposure reversed the adverse effects of cigarette smoke, whereas vascular endothelial growth factor level and nitric oxide synthase activity were unaffected. It is concluded that the detrimental effect of cigarette smoke on ulcer healing is a consequence of reduction of angiogenesis, cell proliferation, and mucus secretion through the depressive action on EGF biosynthesis and its mRNA expression in salivary glands and gastric mucosa.

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“…Moreover, it has been believed that pepsin activity is dependent on the pH of gastric juice and the highest activity is seen at pH 2 and is detectable to a pH 5, although some minimal activity is still seen in pH 5–7 20, 21 . As shown in Table 2 and Figure 2 at day 5, subjects receiving once daily AG 201904‐Z had a reasonable 24‐h acid control beyond this level, while subjects receiving esomeprazole could not achieve a consistent 24‐h acid control especially for the nocturnal period.…”

Section: Discussionmentioning

confidence: 97%