Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have recently reported that basic fibroblast growth factor (bFGF) acts in the brain to inhibit the secretion of gastric acid and pepsin, two major aggressive factors in the pathogenesis of gastric ulcer formation. In the present study, we determined whether or not bFGF has an anti-ulcer action via the central nervous system, using male Wistar rats. The intracisternal injection of bFGF dose-dependently (0.1-1.0 microgram(s)/rat) inhibited the severity of gastric ulcers induced by water-immersion restraint stress or central thyrotropin-releasing hormone. The same doses of peripherally injected bFGF failed to protect the gastric mucosa from these ulcerogenic procedures. These results suggest for the first time that bFGF has a mucosal protective effect through a mechanism involving the central nervous system. It is speculated that this anti-ulcer action of bFGF is, at least in part, dependent upon its gastric antisecretory effect.
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PMID:Central basic fibroblast growth factor inhibits gastric ulcer formation in rats. 190 25

This study evaluated the hypothesis that the dorsal motor nucleus (DMN) of the brainstem may mediate the ulcerogenic and acid-stimulatory effects of thyrotropin-releasing hormone (TRH) in rats. To accomplish this, intra-DMN microinjections of TRH (50 and 500 ng) were performed and their effects on acid secretion and gastric ulcer formation evaluated in the pylorus-ligation model. The high (500 ng), but not the low dose of TRH (50 ng) produced gastric glandular lesions in 64% of the rats with a mean severity index (no. of ulcers/rat) of 6.4 +/- 0.98 and significantly increased gastric acid output. The ulcerogenic and gastric secretory response to intra-DMN TRH was site-specific. We conclude that presynaptic TRH fibers may modulate vagal activity at the level of the DMN and propose that descending TRH pathways may play a role in experimental ulcerogenesis through acid hypersecretion.
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PMID:Thyrotropin-releasing hormone: medullary site of action to induce gastric ulcers and stimulate acid secretion. 313 60