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This study was conducted to examine the hypothesis that basic fibroblast growth factor (bFGF) may have an anti-ulcer action through an acid-independent mechanism. The intracisternal injection of bFGF (1 microgram/10 microliters) significantly attenuated the development of gastric mucosal damage evoked by either subcutaneous indomethacin or intragastric absolute ethanol. On the other hand, intraperitoneally injected bFGF (1 microgram) failed to inhibit the formation of gastric mucosal injury by indomethacin or ethanol. These results suggest that bFGF acts in the brain to exert a gastroprotective action. Since ethanol-induced gastric lesion formation does not depend upon luminal acid, we speculate that an acid-independent mechanism may mediate the anti-ulcer action of central bFGF.
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