Involvement of reactive oxygen species and nitric oxide on gastric ischemia-reperfusion injury in rat: Protective effect of tetrahydrobiopterin.

Ishii, Masakazu; Shimizu, Shunichi; Nawata, Shuichi; Kiuchi, Yuji; Yamamoto, Toshinori

doi:10.1016/s0021-5198(19)34825-5

Cited by 2 publications

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“…In recent years, there has been an increase in the available information concerning the acute gastric mucosal injury induced by I/R, or gastric I/R injury [1][2][3][4] . The investigative key points have focused on the effects of individual factors on gastric mucosal injury induced by gastric I/R, including increase of oxygen free radicals and endothelin level, microvascular dysfunction, polymorphonuclear leukocyte infiltration, nitric oxide release, gastric acid secretion, prostaglandin decrease and so on [5][6][7][8][9][10][11][12][13][14][15] . Some researchers have quested the best methods to protect the gastric mucosa against gastric I/R injury, such as the endothelin converting enzyme inhibitor phosphoramidon [16] , the anti-reactive oxygen species drug, tetrahydrabioptin [9] and the adhesion molecules of antileukocytes [17] .…”

Section: Introductionmentioning

confidence: 99%

Effect and mechanism of β-L-D4A on DNA polymerase α

Yan¹,

Li²,

Ju-Sheng³

et al. 2007

WJG

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Section: Introductionmentioning

confidence: 99%

Effect and mechanism of β-L-D4A on DNA polymerase α

Yan¹,

Li²,

Ju-Sheng³

et al. 2007

WJG

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Roles of NADPH Oxidase in Occurrence of Gastric Damage and Expression of Cyclooxygenase-2 During Ischemia/Reperfusion in Rat Stomachs

Nakagiri

Murakami

2009

J Pharmacol Sci

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Abstract. NADPH oxidase is an enzyme that converts molecular oxygen into reactive oxygen species, which cause severe damage in several organs. Cyclooxygenase (COX)-2 is an inducible enzyme that is important in gastric mucosal defense and repair processes. It is unclear whether NADPH oxidase is related to COX expression in the gastric mucosa, so we investigated the correlation. Under urethane anesthesia, a male Sprague Dawley rat stomach was mounted in an ex-vivo chamber, and ischemia/reperfusion (I/R) was performed through a cannula in the femoral vein. I /R significantly increased NADPH oxidase activity, H 2 O 2 production, and myeloperoxidase (MPO) activity. In contrast, ischemia alone clearly enhanced both NADPH oxidase activity and H 2 O 2 production but not MPO activity. Pretreatment with the NADPH oxidase inhibitor diphenylene iodonium (DPI) suppressed I/R-induced mucosal damage. On the other hand, the selective COX-2 inhibitor rofecoxib exhibited a tendency to enhance the severity of gastric damage induced by I /R, although the selective COX-1 inhibitor SC-560 and the nonselective COX inhibitor indomethacin had no effect. I/R also increased the expression of COX-2, and this increase was suppressed by pretreatment with DPI. These findings suggest that the increase in NADPH oxidase activity is involved in the occurrence of gastric mucosal damage induced by I /R and that this enzyme activity may be causally related to the upregulation of COX-2 during I /R.

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Involvement of reactive oxygen species and nitric oxide on gastric ischemia-reperfusion injury in rat: Protective effect of tetrahydrobiopterin.

Cited by 2 publications

References 0 publications

Effect and mechanism of β-L-D4A on DNA polymerase α

Effect and mechanism of β-L-D4A on DNA polymerase α

Roles of NADPH Oxidase in Occurrence of Gastric Damage and Expression of Cyclooxygenase-2 During Ischemia/Reperfusion in Rat Stomachs

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