A new gastric ulcer model induced by ischemia-reperfusion in the rat: Role of leukocytes on ulceration in rat stomach

Wada, Kouichirou; Kamisaki, Yoshínori; Kitano, Masayuki; Kishimoto, Yosuke; Nakamoto, Kentaro; Itoh, Tadao

doi:10.1016/0024-3205(96)00500-0

Cited by 85 publications

(58 citation statements)

References 17 publications

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“…On the other hand, ischemia-reperfusioninduced gastric injury has been shown to be aciddependent (45,46). Actually, preliminary studies in our laboratory showed that ischemia-reperfusion procedures without intragastric HCl produced much less severe mucosal injury.…”

Section: Discussionmentioning

confidence: 86%

Phosphodiesterase Type IV Inhibitors Prevent Ischemia-Reperfusion-Induced Gastric Injury in Rats

et al. 2004

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Abstract. The effects of selective inhibitors of phosphodiesterase type IV (PDE4) on ischemiareperfusion-induced gastric injuries were investigated in rats. Gastric ischemia was induced by applying a small clamp to the celiac artery, and reoxygenation was performed by removal of the clamp. Ischemia-reperfusion produced gastric hemorrhagic injuries and increased the content of the proinflammatory cytokine tumor necrosis factor-a (TNF-a ) and myeloperoxidase (MPO) activity in gastric mucosa. Rolipram (0.03 -0.3 mg / kg, s.c.) and Ro-20-1724 (0.3 -3 mg/ kg, s.c.) prevented the development of gastric injury in a dose-dependent manner, and it also inhibited the increase in mucosal TNF-a content and MPO activity induced by ischemiareperfusion. The anti-ulcer drug irsogladine (1 -10 mg / kg, p.o.), which is known to possess a PDE4 inhibitory action, also inhibited the gastric injury produced by ischemia-reperfusion, as well as the increase in TNF-a levels and MPO activity. It is concluded that the ability of PDE4 inhibitors to inhibit cytokine TNF-a synthesis and the infiltration of polymorphonuclear leukocytes underlies their gastroprotective effects in ischemia-reperfusion-induced gastric injury. Our experiments suggest that drugs that inhibit PDE4 isoenzyme, such as the anti-ulcer drug irsogladine, may be a useful adjunct therapy for the treatment of the gastric damage that follows ischemia-reperfusion.

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Section: Discussionmentioning

confidence: 86%

Phosphodiesterase Type IV Inhibitors Prevent Ischemia-Reperfusion-Induced Gastric Injury in Rats

et al. 2004

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“…Acute gastric mucosal lesions were produced by I/R (Wada et al, 1996). Briefly, under urethane anesthesia (1.25 g/kg i.p.…”

Section: Methodsmentioning

confidence: 99%

Roles of Cyclooxygenase-2 and Prostacyclin/IP Receptors in Mucosal Defense against Ischemia/Reperfusion Injury in Mouse Stomach

Kotani

Kobata²,

Nakamura³

et al. 2005

J Pharmacol Exp Ther

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We examined the roles of cyclooxygenase (COX) isozymes, prostaglandins (PGs), and their receptors in the mucosal defense against ischemia/reperfusion (I/R)-induced gastric lesions in mice. Male C57BL/6 mice, including wild-type animals and those lacking prostaglandin E 2 (EP)1, EP3, or prostaglandin I 2 (IP) receptors, were used after 18 h of fasting. Under urethane anesthesia, the celiac artery was clamped (ischemia) for 30 min, and then reperfusion was achieved for 60 min through the removal of the clamp, and the stomach was examined for lesions. I/R produced hemorrhagic gastric lesions in wild-type mice. The severity of lesions was significantly increased by pretreatment with indomethacin (a nonselective COX inhibitor) and rofecoxib (a selective COX-2 inhibitor) but not 5-(4-chlorophenyl)-1-(4-methoxyphenyl)-3-(trifluoromethyl)-1H-pyrazole (SC-560; a selective COX-1 inhibitor). The expression of COX-2 mRNA was up-regulated in the stomach following I/R but not by sham operation or ischemia alone. The ulcerogenic response was markedly aggravated in IP receptor knockout mice but not those lacking EP1 or EP3 receptors. I/R increased the levels of 6-keto-PGF 1␣ and PGE 2 in the stomach of wildtype mice, and this response was attenuated by indomethacin and rofecoxib but not SC-560. Pretreatment of wild-type mice with iloprost, a prostacyclin (PGI 2 ) analog, significantly prevented the I/R-induced gastric lesions in the absence and presence of indomethacin or rofecoxib. PGE 2 also reduced the severity of I/R-induced gastric lesions, yet the effect was much less pronounced than that of iloprost. These results suggest that endogenous PGs derived from COX-2 play a crucial role in gastric mucosal defense during I/R, and this action is mainly mediated by PGI 2 through the activation of IP receptors.

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“…Gastric I/R injury was induced according to Wada et al, (1996). Briefly, under anesthesia with a mixture of ketamine and xylazine (60+15 mg/kg, i.p.…”

Section: Animal Grouping and Experimental Proceduresmentioning

confidence: 99%

A preliminary study of the anti-inflammatory and anti-apoptotic effects of crocin against gastric ischemia-reperfusion injury in rats

Mard

Nikraftar

Farbood

et al. 2015

Braz. J. Pharm. Sci.

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The aim of the present study was to investigate the protective effect of crocin on gastric mucosal lesions caused by ischemia-reperfusion (I/R) injury in rats. Thirty-two male rats were randomly divided into sham, I/R, I/R + crocin pretreatment and crocin alone groups. To induce I/R lesions, the celiac artery was clamped for 30 min, and the clamp was then removed to allow reperfusion for 3 h. Crocin-pretreated rats received crocin (15 mg/kg, i.p.) 30 min prior to the induction of I/R injury. Samples of gastric mucosa were collected to quantify the protein expression of caspase-3, an apoptotic factor, and inducible nitric oxide synthase (iNOS), a pro-inflammatory protein, by Western blot. Pretreatment with crocin decreased the total area of gastric lesions and decreased the protein expression levels of caspase-3 and iNOS induced by I/R injury. Our findings showed a protective effect of crocin in gastric mucosa against I/R injury. This effect of crocin was mainly mediated by reducing the protein expression of iNOS and caspase-3. Uniterms:Crocin/protective effect. Gastric mucosal/lesions/ ischemia-reperfusion. Gastric lesions/ treatment/experimental study. Caspase-3. Inducible nitric oxide synthase.O objetivo do presente estudo foi investigar o efeito protetor da crocina em lesões da mucosa gástrica causadas por isquemia-reperfusão (I/R) em ratos. Trinta e dois ratos machos aleatoriamente divididos em grupos de ratos normais, operados como controle, I/R. I/R + pré-tratamento com crocina e crocina sozinha. Para induzir lesões I/R, a artéria celíaca foi grampeada durante 30 minutos e, em seguida, o grampo foi removido para permitir a reperfusão por 3 h. Ratos com pré-tratamento com crocina receberam crocina (15 mg/kg, ip) 30 minutos antes da indução do dano I/R. Amostras de mucosa gástrica foram coletadas para qiuantificar a expressão da proteína da caspase-3, o fator apoptótico, e óxido nítrico sintase induzível (iNOS), uma proteína anti-inflamatória, pela técnica de Western Blot. O pré-tratamento com crocina diminuiu a área total de lesões gástricas e a expressão de níveis de caspase-3 e iNOS induzidas pelo dano I/R. Nossos resultados mostraram o efeito protetor da crocina na mucosa gástrica contra o dano I/R. Este efeito foi mediado, principalmente, por diminuição da expressão das proteínas iNOS e caspase-3.Unitermos: Crocina/efeito protetor. Mucosa gástrica/lesão/isquemia-reperfusão. Lesões gástricas/ tratamento/estudo experimental. Caspase-3. Óxido nítrico sintase induzível.

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A new gastric ulcer model induced by ischemia-reperfusion in the rat: Role of leukocytes on ulceration in rat stomach

Cited by 85 publications

References 17 publications

Phosphodiesterase Type IV Inhibitors Prevent Ischemia-Reperfusion-Induced Gastric Injury in Rats

Phosphodiesterase Type IV Inhibitors Prevent Ischemia-Reperfusion-Induced Gastric Injury in Rats

Roles of Cyclooxygenase-2 and Prostacyclin/IP Receptors in Mucosal Defense against Ischemia/Reperfusion Injury in Mouse Stomach

A preliminary study of the anti-inflammatory and anti-apoptotic effects of crocin against gastric ischemia-reperfusion injury in rats

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