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Rebamipide, a mucoprotective drug, inhibits NSAIDs-induced gastric mucosal injury: possible involvement of the downregulation of 15-hydroxyprostaglandin dehydrogenase.

Tanigawa T, Watanabe T, Ohkawa F, Nadatani Y, Otani K, Machida H, Okazaki H, Yamagami H, Watanabe K, Tominaga K, Fujiwara Y, Takeuchi K, Arakawa T - J Clin Biochem Nutr (2011)

Bottom Line: Rebamipide did not affect the expression of cyclooxygenase-1 in the gastric tissue.Rebamipide did not increase prostaglandin E(2) production in the gastric tissue; however, it induced a 1.4-fold increase in the concentration of prostaglandin E(2) in the gastric tissue as compared to vehicle-treated control mice.These results suggest that the suppressive effect of rebamipide on non-steroidal anti-inflammatory drugs-induced gastric mucosal injury can be attributed to reduced 15-hydroxyprostaglandin dehydrogenase expression, which increases the prostaglandin E(2) concentration in the gastric tissue.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka City, Osaka 545-8585, Japan.

ABSTRACT
Prostaglandin E(2) plays an important role in the maintenance of gastric mucosal integrity. The level of biologically active prostaglandin E(2) in the tissue is regulated by the balanced expression of its synthetic enzymes, such as cyclooxygenase, and its catabolic enzyme, 15-hydroxyprostaglandin dehydrogenase. We examined the effect of rebamipide, a mucoprotective drug, on prostaglandin E(2) production and metabolism in the gastric tissue and its effect on indomethacin-induced gastric mucosal injury in mice. Rebamipide suppressed indomethacin-induced gastric mucosal injury. Suppressive effect of rebamipide on indomethacin-induced gastric mucosal injury was also observed in cyclooxygenase-2-knockout mice. The mice that were treated with rebamipide showed a 2-fold increase in cyclooxygenase-2 mRNA expression in the gastric tissue, whereas 15-hydroxyprostaglandin dehydrogenase mRNA expression markedly decreased as compared to vehicle-treated control mice. Rebamipide did not affect the expression of cyclooxygenase-1 in the gastric tissue. Rebamipide did not increase prostaglandin E(2) production in the gastric tissue; however, it induced a 1.4-fold increase in the concentration of prostaglandin E(2) in the gastric tissue as compared to vehicle-treated control mice. These results suggest that the suppressive effect of rebamipide on non-steroidal anti-inflammatory drugs-induced gastric mucosal injury can be attributed to reduced 15-hydroxyprostaglandin dehydrogenase expression, which increases the prostaglandin E(2) concentration in the gastric tissue.

No MeSH data available.


Related in: MedlinePlus

The effect of rebamipide on COX-1, COX-2 and 15-PGDH mRNA expression in the gastric tissue. Mice were given rebamipide (30 or 100 mg/kg) p.o. and killed 4 h later. Data are presented as mean ± SE for 4–6 mice.
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Figure 2: The effect of rebamipide on COX-1, COX-2 and 15-PGDH mRNA expression in the gastric tissue. Mice were given rebamipide (30 or 100 mg/kg) p.o. and killed 4 h later. Data are presented as mean ± SE for 4–6 mice.

Mentions: The mice that were treated with 100 mg/kg BW of rebamipide showed a 2-fold increase in COX-2 mRNA expression in the gastric tissue, while 15-PGDH mRNA expression decreased by 26% or 89% in the mice treated with 30 mg/kg BW or 100 mg/kg BW of rebamipide, respectively, compared with vehicle-treated control mice. Rebamipide did not affect COX-1 mRNA expression (Fig. 2).


Rebamipide, a mucoprotective drug, inhibits NSAIDs-induced gastric mucosal injury: possible involvement of the downregulation of 15-hydroxyprostaglandin dehydrogenase.

Tanigawa T, Watanabe T, Ohkawa F, Nadatani Y, Otani K, Machida H, Okazaki H, Yamagami H, Watanabe K, Tominaga K, Fujiwara Y, Takeuchi K, Arakawa T - J Clin Biochem Nutr (2011)

The effect of rebamipide on COX-1, COX-2 and 15-PGDH mRNA expression in the gastric tissue. Mice were given rebamipide (30 or 100 mg/kg) p.o. and killed 4 h later. Data are presented as mean ± SE for 4–6 mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3045688&req=5

Figure 2: The effect of rebamipide on COX-1, COX-2 and 15-PGDH mRNA expression in the gastric tissue. Mice were given rebamipide (30 or 100 mg/kg) p.o. and killed 4 h later. Data are presented as mean ± SE for 4–6 mice.
Mentions: The mice that were treated with 100 mg/kg BW of rebamipide showed a 2-fold increase in COX-2 mRNA expression in the gastric tissue, while 15-PGDH mRNA expression decreased by 26% or 89% in the mice treated with 30 mg/kg BW or 100 mg/kg BW of rebamipide, respectively, compared with vehicle-treated control mice. Rebamipide did not affect COX-1 mRNA expression (Fig. 2).

Bottom Line: Rebamipide did not affect the expression of cyclooxygenase-1 in the gastric tissue.Rebamipide did not increase prostaglandin E(2) production in the gastric tissue; however, it induced a 1.4-fold increase in the concentration of prostaglandin E(2) in the gastric tissue as compared to vehicle-treated control mice.These results suggest that the suppressive effect of rebamipide on non-steroidal anti-inflammatory drugs-induced gastric mucosal injury can be attributed to reduced 15-hydroxyprostaglandin dehydrogenase expression, which increases the prostaglandin E(2) concentration in the gastric tissue.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka City, Osaka 545-8585, Japan.

ABSTRACT
Prostaglandin E(2) plays an important role in the maintenance of gastric mucosal integrity. The level of biologically active prostaglandin E(2) in the tissue is regulated by the balanced expression of its synthetic enzymes, such as cyclooxygenase, and its catabolic enzyme, 15-hydroxyprostaglandin dehydrogenase. We examined the effect of rebamipide, a mucoprotective drug, on prostaglandin E(2) production and metabolism in the gastric tissue and its effect on indomethacin-induced gastric mucosal injury in mice. Rebamipide suppressed indomethacin-induced gastric mucosal injury. Suppressive effect of rebamipide on indomethacin-induced gastric mucosal injury was also observed in cyclooxygenase-2-knockout mice. The mice that were treated with rebamipide showed a 2-fold increase in cyclooxygenase-2 mRNA expression in the gastric tissue, whereas 15-hydroxyprostaglandin dehydrogenase mRNA expression markedly decreased as compared to vehicle-treated control mice. Rebamipide did not affect the expression of cyclooxygenase-1 in the gastric tissue. Rebamipide did not increase prostaglandin E(2) production in the gastric tissue; however, it induced a 1.4-fold increase in the concentration of prostaglandin E(2) in the gastric tissue as compared to vehicle-treated control mice. These results suggest that the suppressive effect of rebamipide on non-steroidal anti-inflammatory drugs-induced gastric mucosal injury can be attributed to reduced 15-hydroxyprostaglandin dehydrogenase expression, which increases the prostaglandin E(2) concentration in the gastric tissue.

No MeSH data available.


Related in: MedlinePlus