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Vol. 296, Issue 1, 48-56, January 2001
Departments of Applied Pharmacology (S.T., Y.K.) and
Biopharmaceutics (S.T., T.F., T.U., A.Y.), Kyoto Pharmaceutical
University, Misasagi, Yamashina, Kyoto, Japan
FR167653 was discovered as a cytokine production inhibitor, but its
target molecule has remained unclear. We examined the effect of
FR167653 on activities of purified protein kinases. FR167653 dose
dependently inhibited p38
mitogen-activated protein kinase activity
without affecting the activities of other kinases. FR167653 had no
effect on cyclooxygenase (COX)-1 or COX-2 activities, whereas SB203580
inhibited them. FR167653 suppressed endogenous p38 kinase activity in
interleukin-1-stimulated NRK-F cells. These results indicate that
FR167653 is a p38 kinase-selective inhibitor without affecting COX
activity. To evaluate the role of p38 kinase in Helicobacter
pylori gastritis, we therefore examined the effect of FR167653
on H. pylori-induced gastritis in Mongolian gerbils. H. pylori infection activated p38 kinase in the gastric
mucosa and caused neutrophil infiltration from 2 and 3 weeks of
infection, respectively. At 4 weeks, severe mucosal inflammation with
erosive injury was observed. When FR167653 was administered to
H. pylori-infected gerbils from 2 weeks, both neutrophil
infiltration and mucosal injury at 4 weeks were significantly
prevented. FR167653 markedly reduced the H.
pylori-induced increase in endogenous p38 kinase activity in
the gastric mucosa, and also significantly inhibited neutrophil
chemokine production. In contrast, the drug did not affect H.
pylori colonization or acid secretion. FR167653 did not cause
any pathological change in the gastric mucosa of normal animals. These
results indicate that p38 kinase plays a crucial role in H.
pylori-induced gastritis in Mongolian gerbils.
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