Gastric mucosal protection against ethanol by EP2 and EP4 signaling through the inhibition of leukotriene C4 production.

Gastric mucosal protection against ethanol by EP2 and EP4 signaling through the inhibition of leukotriene C4 production. Research Abstract Details 

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Gastric mucosal protection against ethanol by EP2 and EP4 signaling through the inhibition of leukotriene C4 production. Abstract Text:

Youichiro Hattori,Takashi Ohno,Takako Ae,Takeo Saeki,Katsuharu Arai,Sumito Mizuguchi,Katsunori Saigenji,Masataka Majima,Youichiro Hattori,Takashi Ohno,Takako Ae,Takeo Saeki,Katsuharu Arai,Sumito Mizuguchi,Katsunori Saigenji,Masataka Majima,Youichiro Hattori,Takashi Ohno,Takako Ae,Takeo Saeki,Katsuharu Arai,Sumito Mizuguchi,Katsunori Saigenji,Masataka Majima,

Prostaglandin (PG)E derivatives are widely used for treating gastric mucosal injury. PGE receptors are classified into four subtypes, EP(1), EP(2), EP(3), and EP(4). We have tested which EP receptor subtypes participate in gastric mucosal protection against ethanol-induced gastric mucosal injury and clarified the mechanisms of such protection. The gastric mucosa of anesthetized rats was perfused at 2 ml/min with physiological saline, agonists for EP(1), EP(2), EP(3), and EP(4), or 50% ethanol, using a constant-rate pump connected to a cannula placed in the esophagus. The gastric microcirculation of the mucosal base of anesthetized rats was observed by transillumination through a window made by removal of the adventitia and muscularis externa. PGE(2) and subtype-specific EP agonists were applied to the muscularis mucosae at the window. Application of 50% ethanol dilated the mucosal arterioles and constricted the collecting venules. Collecting venule constriction by ethanol was completely inhibited by PGE(2) and by EP(2) and EP(4) agonists (100 nM) but not by an EP(1) or an EP(3) agonist. Ethanol-induced mucosal injury was also inhibited by EP(2) and EP(4) agonists. When leukotriene (LT)C(4) levels in the perfusate of the gastric mucosa were determined by ELISA, intragastric ethanol administration elevated the LTC(4) levels sixfold from the basal levels. These elevated levels were significantly (60%) reduced by both EP(2) and EP(4) agonists but not by other EP agonists. Since LTC(4) application at the window constricted collecting venules strongly, and an LTC antagonist reduced ethanol-induced mucosal injury, reductions in LTC(4) generation in response to EP(2) and EP(4) receptor signaling may be relevant to the protective action of PGE(2). The present results indicate that EP(2) and EP(4) receptor signaling inhibits ethanol-induced gastric mucosal injury through cancellation of collecting venule constriction by reducing LTC(4) production.

Gastric mucosal protection against ethanol by EP2 and EP4 signaling through the inhibition of leukotriene C4 production. Publishing Authors By Initials

Y Hattori,T Ohno,T Ae,T Saeki,K Arai,S Mizuguchi,K Saigenji,M Majima,Y Hattori,T Ohno,T Ae,T Saeki,K Arai,S Mizuguchi,K Saigenji,M Majima,Y Hattori,T Ohno,T Ae,T Saeki,K Arai,S Mizuguchi,K Saigenji,M Majima,

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Gastric mucosal protection against ethanol by EP2 and EP4 signaling through the inhibition of leukotriene C4 production. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: American journal of physiology. Gastrointestinal a

VOLUME: 294

Page Numbers: G80-7

Journal Abbreviation: Am. J. Physiol. Gastrointest.

ISSN: 0193-1857

DAY: 18

MONTH: 10

YEAR: 2007

Gastric mucosal protection against ethanol by EP2 and EP4 signaling through the inhibition of leukotriene C4 production. Information

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LANGUAGE: eng

NlmUniqueID: 100901227

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AFFILIATION: Dept. of Pharmacology, Kitasato Univ. School of Medicine, Sagamihara, Kanagawa 228-8555, Japan. mmajima@med.kitasato-u.ac.jp).

Country: United States

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MEDLINETA: Am J Physiol Gastrointest Live

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