Abstract
Here we show that the vasoactive peptide amylin protects against reserpine-induced gastric injury in the rat, resulting in lower score of gastric lesions. Hepatocyte growth factor (HGF), its c-Met receptor and cyclooxygenase-2 (COX-2) expression, usually increased in course of reserpine-induced gastric damage, was decreased in rats treated with amylin. Pretreatment with the specific amylin receptor antagonist AC187 abrogated the gastroprotective effects of amylin and restored high expression levels of HGF, c-Met and COX-2. Our data suggest that protective effects of amylin upon the gastric mucosa are specific and eventually involve modulation of HGF, c-Met and COX-2 expression.
MeSH terms
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Amyloid / pharmacology*
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Animals
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Anti-Ulcer Agents / pharmacology
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Blotting, Western
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Cyclooxygenase 2 / metabolism
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Gastric Mucosa / drug effects
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Gastric Mucosa / metabolism
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Gastric Mucosa / pathology
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Hepatocyte Growth Factor / metabolism
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Islet Amyloid Polypeptide
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MAP Kinase Kinase 4 / metabolism
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Male
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Peptide Fragments / pharmacology
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Phosphorylation / drug effects
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Proto-Oncogene Proteins c-met / metabolism
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Rats
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Rats, Sprague-Dawley
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Receptors, Islet Amyloid Polypeptide
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Receptors, Peptide / antagonists & inhibitors
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Reserpine / toxicity*
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Stomach Ulcer / chemically induced
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Stomach Ulcer / pathology
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Stomach Ulcer / prevention & control*
Substances
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Amyloid
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Anti-Ulcer Agents
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Islet Amyloid Polypeptide
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Peptide Fragments
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Receptors, Islet Amyloid Polypeptide
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Receptors, Peptide
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AC 187
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Hepatocyte Growth Factor
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Reserpine
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Cyclooxygenase 2
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Proto-Oncogene Proteins c-met
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MAP Kinase Kinase 4