Cytoprotection by prostaglandins

Robert, André

doi:10.1016/0016-5085(79)90235-x

Cited by 1,000 publications

(399 citation statements)

References 30 publications

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“…Most importantly, gastric lesions were inhibited by PGE 2 at the dose that in our preliminary study had little effect on gastric acid secretion in rats equipped with chronic gastric fistulas [4]. This suggests that the gastroprotective effect of PGE 2 is probably not related to gastric acid secretion, but represents the genuine cytoprotective properties of these arachidonate metabolites according to the concept originally pioneered by Robert et al [5]. PGE 2 must have beneficial effect besides of its recognized ability to improve blood flow, since in this model blood flow was impaired due to L-AV occlusion.…”

Section: Resultsmentioning

confidence: 56%

Acute gastric lesions induced by the administration of histamine to rats with partial vascular occlusion: evidence for the gastroprotective effect of prostaglandin

et al. 2009

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Section: Resultsmentioning

confidence: 56%

Acute gastric lesions induced by the administration of histamine to rats with partial vascular occlusion: evidence for the gastroprotective effect of prostaglandin

et al. 2009

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“…At present, it is considered that endogenous prostaglandins (PGs) play a key role in adaptive cytoprotection. [15][16][17][18] Recent attention has also been focused on the relationship between HSPs and adaptive cytoprotection. 4,19,20 Yeomans et al 21 reported that HSPs were expressed as a result of cellular damage in rats with injury to the gastric mucosa induced by diclofenac; however, they indicated that the expression of HSPs was probably not the principal mechanism of adaptation.…”

Section: Discussionmentioning

confidence: 99%

Injury to the Gastric Mucosa and Cellular Dynamics in a Rat Model of Duodenogastric Reflux: The Possible Significance of Gastrin Induction and a Heat Shock Protein

Kubo¹,

Noguchi²,

Takeno³

et al. 2000

Surgery Today

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Injury to the gastric mucosa caused by duodenogastric reflux (DGR) is often encountered after gastrectomy or truncal vagotomy (V) with pyloroplasty. This study was designed to investigate the histological features of the gastric mucosa under such conditions. A rat model of DGR and DGR+V was established and the thickness of the oxyntic mucosa was measured. Cellular dynamics in the presence of injury to the gastric mucosa caused by DGR were investigated by the immunohistochemical staining of bromodeoxyuridine (BrdU) and heat shock protein 70 (HSP70). The relationship between persistent hypergastrinemia and mucosal injury was also studied. Duodenogastric reflux activated the intracellular induction of HSP70 in our rat model of DGR. Hypergastrinemia was noted in the V group. Compared with values from the DGR group, the numbers of BrdU-labeled cells increased, the glandular proliferation zone expanded, and the thickness of the oxyntic mucosa was significantly higher in the DGR+V group. Compared with the DGR group, there was greater induction of HSP in the DGR+V group during the acute stage. This finding suggests that denervation of the gastric mucosa and hypergastrinemia after vagotomy may be associated with the expression of HSP.

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“…Both prostaglandins and trefoil peptides have cytoprotective functions in the gastric mucosa [44,45], and it has been suggested that the actions of these two families may be linked [46]. A common linkage may be one or more members of the prostaglandin and peroxisome proliferator-activated receptors (PPARs) transcription factor family of nuclear receptors, which are involved in modulating cell growth, differentiation and infl ammation in the gut and elsewhere [47,48].…”

Section: Prostaglandins and Peroxisome Proliferatoractivated Receptorsmentioning

confidence: 99%

Trefoil factors

Baus-Lončar

Giraud

2005

Cell. Mol. Life Sci.

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The expression of trefoil peptides and their biological consequences are regulated in a multifactorial fashion, and much more work is required in order to fully understand the underlying molecular mechanisms. Central to this will be the identification and functional analysis of trefoil peptide receptors and the full complement of binding proteins. This review summarizes the often fragmentary information available on the environmental, chemical and local regulatory molecules that control trefoil gene expression. Special attention is paid to the nature of the signaling cascades that are activated and the binding proteins that modulate gene transcription. Epigenetic regulation of trefoil gene expression, particularly the role of (de)methylation is described, and the signaling pathways downstream of trefoil peptide activation of target cells are enumerated, as are their physiological and pathological outcomes.

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Cytoprotection by prostaglandins

Cited by 1,000 publications

References 30 publications

Acute gastric lesions induced by the administration of histamine to rats with partial vascular occlusion: evidence for the gastroprotective effect of prostaglandin

Acute gastric lesions induced by the administration of histamine to rats with partial vascular occlusion: evidence for the gastroprotective effect of prostaglandin

Injury to the Gastric Mucosa and Cellular Dynamics in a Rat Model of Duodenogastric Reflux: The Possible Significance of Gastrin Induction and a Heat Shock Protein

Trefoil factors

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