L‐365,260 inhibits <i>in vitro</i> acid secretion by interacting with a PKA pathway

Oiry, Catherine; Pannequin, Julie; Cormier, Anne; Galleyrand, Jean-Claude; Martinez, Jean

doi:10.1038/sj.bjp.0702505

Cited by 5 publications

(4 citation statements)

References 33 publications

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“…In addition, L365260 is believed to be specificity for the CCK-2 receptor. 25,26 In our research, L365260, a CCK-2 receptor antagonist, indeed down-regulated the expression of CCK-2R. There may be an uncharted mechanism that could explain this effect.…”

Section: Discussionsupporting

confidence: 51%

Gastrin attenuates ischemia-reperfusion-induced intestinal injury in rats

Liu

Luo

Cheng

et al. 2016

Exp Biol Med (Maywood)

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Intestinal ischemia-reperfusion (I/R) injury is a devastating complication when the blood supply is reflowed in ischemic organs. Gastrin has critical function in regulating acid secretion, proliferation, and differentiation in the gastric mucosa. We aimed to determine whether gastrin has an effect on intestinal I/R damage. Intestinal I/R injury was induced by 60-min occlusion of the superior mesenteric artery followed by 60-min reperfusion, and the rats were induced to be hypergastrinemic by pretreated with omeprazole or directly injected with gastrin. Some hypergastrinemic rats were injected with cholecystokinin-2 (CCK-2) receptor antagonist prior to I/R operation. After the animal surgery, the intestine was collected for histological analysis. Isolated intestinal epithelial cells or crypts were harvested for RNA and protein analysis. CCK-2 receptor expression, intestinal mucosal damage, cell apoptosis, and apoptotic protein caspase-3 activity were measured. We found that high gastrin in serum significantly reduced intestinal hemorrhage, alleviated extensive epithelial disruption, decreased disintegration of lamina propria, downregulated myeloperoxidase activity, tumor necrosis factor-a, and caspase-3 activity, and lead to low mortality in response to I/R injury. On the contrary, CCK-2 receptor antagonist L365260 could markedly impair intestinal protection by gastrin on intestinal I/R. Severe edema of mucosal villi with severe intestinal crypt injury and numerous intestinal villi disintegrated were observed again in the hypergastrinemic rats with L365260. The survival in the hypergastrinemic rats after intestinal I/R injury was shortened by L365260. Finally, gastrin could remarkably upregulated intestinal CCK-2 receptor expression. Our data suggest that gastrin by omeprazole remarkably attenuated I/R induced intestinal injury by enhancing CCK-2 receptor expression and gastrin could be a potential mitigator for intestinal I/R damage in the clinical setting.

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Section: Discussionsupporting

confidence: 51%

Gastrin attenuates ischemia-reperfusion-induced intestinal injury in rats

Liu

Luo

Cheng

et al. 2016

Exp Biol Med (Maywood)

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“…By using sensitive techniques used previously by our group on various cellular models (Oiry et al, 1999;Poosti et al, 2000), we have tested the effect of G-7 on intracellular inositol phosphates accumulation (Fig. 6A) and cAMP production (Fig.…”

Section: Role Of New Gastrin Binding Site On U373 Cellsmentioning

confidence: 99%

C-Terminal Heptapeptide of Gastrin Inhibits Astrocytomas Motility by Interacting with a New Gastrin Binding Site

Pannequin¹,

Oiry²,

Morel³

et al. 2002

J Pharmacol Exp Ther

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It is well known that the amidated C-terminal part of gastrin is crucial for its interaction with the classical seven transmembrane domain receptors CCK-1 or CCK-2. Nevertheless, over the past 10 years, several groups have characterized new binding sites using peptides related to gastrin (particularly glycineextended forms of gastrin) on various tumoral and nontumoral cell lines. In the present study, we focused on the human astrocytic tumoral cell line U373. Although it has been described that gastrin was able to inhibit the motility of these cells, we were unable to detect any classical CCK/gastrin receptor.On the other hand, by using the radiolabeled C-terminal heptapeptide of gastrin ( 125

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“…42 The three most important mediators, namely acetylcholine, gastrin, and histamine, interact with specific receptors located at the basolateral membrane of the parietal cells that stimulate gastric acid secretion. 43 The regulation of gastric acid secretion by the parietal cells is an important factor in the pathogenesis of peptic ulcer. Therefore, the inhibition of gastric acid secretion is a key therapeutic target for the ulcer diseases.…”

Section: Resultsmentioning

confidence: 99%

Evaluation of Anti-Ulcer Properties of the Stem-Bark Fractions of Khaya senegalensis (Desr.) A. Jussin Albino Rats

Suleiman¹,

.²,

Mikail³

et al. 2019

TJNPR

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Article history:preliminary evaluation of crude methanol stem-bark extract of the plant revealed potent antiulcer properties. 21 Although much progress has been made in the management of H. pylori infection in gastric ulcer due to the widespread use of antisecretory drugs and antibiotics, increasing antimicrobial resistance has posed a great threat to its eradication. 22 Furthermore, emerging causes of peptic ulcers other than H. pylori and NSAIDs are imposing diagnostic and therapeutic challenges. Therefore, the aim of this study was to investigate the anti-ulcer effects of the stem-bark fractions of K. senegalensis in rats.

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L‐365,260 inhibits in vitro acid secretion by interacting with a PKA pathway

Cited by 5 publications

References 33 publications

Gastrin attenuates ischemia-reperfusion-induced intestinal injury in rats

Gastrin attenuates ischemia-reperfusion-induced intestinal injury in rats

C-Terminal Heptapeptide of Gastrin Inhibits Astrocytomas Motility by Interacting with a New Gastrin Binding Site

Evaluation of Anti-Ulcer Properties of the Stem-Bark Fractions of Khaya senegalensis (Desr.) A. Jussin Albino Rats

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