Pancreatic spasmolytic polypeptide protects the gastric mucosa but does not inhibit acid secretion or motility

1997 ◽  
Vol 273 (1) ◽  
pp. G112-G117 ◽  
Author(s):  
C. McKenzie ◽  
T. Marchbank ◽  
R. J. Playford ◽  
W. Otto ◽  
L. Thim ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Mucosal Damage ◽  
Inhibitory Effect ◽  
Gastric Mucosal Damage ◽  
Conscious Rat ◽  
Immature Rat ◽  
Trefoil Peptide ◽  
Spasmolytic Polypeptide ◽  
Evoked Contractions

The objectives of these studies were to examine whether the trefoil peptide porcine pancreatic spasmolytic polypeptide (PSP) had gastric mucosal protectant properties similar to its human equivalent human spasmolytic polypeptide (hSP) and to confirm the antisecretory and antimotility action of the peptide. PSP and recombinant hSP reduced gastric mucosal damage caused by a combination of subcutaneous indomethacin and restraint stress in the conscious rat. At a dose of 500 micrograms/kg bolus plus 500 micrograms.kg-1.h-1 sc, PSP significantly reduced the total area of damage by 58%. PSP at a dose of 150 micrograms/kg iv had no inhibitory effect on pentagastrin-stimulated gastric acid secretion in the perfused stomachs of anesthetized rats. This lack of antisecretory activity was confirmed in vitro using an isolated stomach preparation from the immature rat. PSP and hSP at concentrations up to 800 nM did not inhibit electrically or chemically evoked contractions of the guinea pig ileum and duodenum in vitro. Thus antisecretory and antimotility actions do not underlie the mucosal protectant properties of PSP. PSP did, however, stimulate cell migration, and this may, at least in part, account for its protectant properties.

A new in vitro model for ethanol-induced gastric mucosal damage

1999 ◽  
Vol 41 (4) ◽  
pp. 167-172 ◽  
Author(s):  
Yassir M.Al-Mulla Hummadi ◽  
Rafid A Najim ◽  
Imad B Farjou
Keyword(s):  
In Vitro Model ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Vitro Model

scholarly journals Lack of Small Intestinal Dysbiosis Following Long-Term Selective Inhibition of Cyclooxygenase-2 by Rofecoxib in the Rat

Cells ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 251 ◽  
Author(s):  
Bernadette Lázár ◽  
Gábor Brenner ◽  
András Makkos ◽  
Mihály Balogh ◽  
Szilvia László ◽  
...  
Keyword(s):  
Selective Inhibition ◽  
Mucosal Damage ◽  
Inhibitory Effect ◽  
Intestinal Dysbiosis ◽  
Bowel Diseases ◽  
Direct Inhibitory Effect ◽  
Cox 2 ◽  
Small Intestinal

Intestinal dysbiosis is linked to numerous gastrointestinal disorders, including inflammatory bowel diseases. It is a question of debate if coxibs, selective inhibitors of cyclooxygenase (COX)-2, cause dysbiosis. Therefore, in the present study, we aimed to determine the effect of long-term (four weeks) selective inhibition of COX-2 on the small intestinal microbiota in the rat. In order to avoid mucosal damage due to topical effects and inflammation-driven microbial alterations, rofecoxib, a nonacidic compound, was used. The direct inhibitory effect of rofecoxib on the growth of bacteria was ruled out in vitro. The mucosa-sparing effect of rofecoxib was confirmed by macroscopic and histological analysis, as well as by measuring the intestinal levels of cytokines and tight junction proteins. Deep sequencing of bacterial 16S rRNA revealed that chronic rofecoxib treatment had no significant influence on the composition and diversity of jejunal microbiota. In conclusion, this is the first demonstration that long-term selective inhibition of COX-2 by rofecoxib does not cause small intestinal dysbiosis in rats. Moreover, inhibition of COX-2 activity is not likely to be responsible per se for microbial alterations caused by some coxibs, but other drug-specific properties may contribute to it.

scholarly journals Terazosin Stimulates Pgk1 to Remedy Gastrointestinal Disorders

2021 ◽  
Vol 23 (1) ◽  
pp. 416
Author(s):  
Jingjing Liu ◽  
Wenyang Zhao ◽  
Chun Li ◽  
Tongyu Wu ◽  
Liang Han ◽  
...  
Keyword(s):  
Gastrointestinal Disease ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Health Concern ◽  
Disease Treatment ◽  
Atp Production ◽  
Anti Inflammation ◽  
Clinical Drug

Gastrointestinal disease is the most common health concern that occurs due to environmental, infectious, immunological, psychological, and genetic stress. Among them, the most frequent diseases are gastric ulcer (GU) and ulcerative colitis (UC). DSS-induced UC and ethanol-stimulated GU models resemble the pathophysiology of human gastrointestinal disease. The current study was designed to explore the anti-oxidation, anti-inflammation, anti-cell death properties of terazosin, an α-adrenergic receptor antagonist, in vivo and in vitro. Our results indicate that terazosin dramatically activates Pgk1, and upregulates glycose metabolism, evidenced by the enhanced ATP production and higher LDH enzymatic activity. Also, terazosin significantly enhances p-AKT expression and inhibits NF-κB p65 activation through abrogating the phosphorylation of IKBα, as well as lowers Caspase-1 and GSDMD expression. The findings in this study demonstrate that terazosin exhibits anti-inflammatory effects by downregulating NF-κB-GSDMD signal pathway, along with enhancing glycolysis for gastrointestinal disease treatment. Meanwhile, we also find terazosin ameliorates ethanol-induced gastric mucosal damage in mice. Collectively, as a clinical drug, terazosin should be translated into therapeutics for gastrointestinal disease soon.

scholarly journals Gastroprotective Effect of Ethanol Extracts from Bark of Magnolia officinalis on Ethanol-Induced Gastric Mucosal Damage in Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Xiao Wang ◽  
Shu Fu ◽  
Chen Zhang ◽  
Xin Nie ◽  
Wan Liao ◽  
...  
Keyword(s):  
Gastric Ulcer ◽  
Periodic Acid ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Gastric Injury ◽  
Dependent Manner ◽  
Gastroprotective Effect ◽  
Ethanol Extracts ◽  
Magnolia Officinalis

Background. Magnolia officinalis Rehd. and Wils. is widely used in Asian countries because of its multiple pharmacological effects. This study investigated the gastroprotective effect and mechanisms of the ethanol extracts from the bark of Magnolia officinalis (MOE) against ethanol-induced gastric mucosal damage in rats. Methods. MOE was prepared by reflux extraction with 70% ethanol, and its main compounds were analyzed by UPLC-Q-Exactive Orbitrap-MS. DPPH, ABTS, and FRAP methods were used to evaluate the antioxidant capacity of MOE in vitro. The gastroprotective effects of MOE were evaluated by the area of gastric injury, H&E (hematoxylin-eosin), and PAS (periodic acid-Schiff). The mechanism was explored by measuring the levels of cytokines and protein in the NF-κB signaling pathway. Results. 30 compounds were identified from MOE, mainly including lignans and alkaloids. MOE presented a high antioxidant activity in several oxidant in vitro systems. Gastric ulcer index and histological examination showed that MOE reduced ethanol-induced gastric mucosal injury in a dose-dependent manner. MOE pretreatment significantly restored the depleted activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) enzymes, reduced malondialdehyde (MDA), and prostaglandin E2 (PGE2) levels in the gastric tissue in rats. In addition, MOE also inhibited the activation of nuclear factor kappa B (NF-κB) pathway and decreased the production of proinflammatory cytokines. Conclusions. The gastroprotective effect of MOE was attributed to the inhibition of oxidative stress and the NF-κB inflammatory pathway. The results provided substantial evidence that MOE could be a promising phytomedicine for gastric ulcer prevention.

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