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pubmed-article:15808664pubmed:abstractTextProstaglandin E(2) (PGE(2)) mediates a variety of both innate and adaptive immunity responses through 4 distinct receptors, EP1-4. Recent studies have suggested the physiological and pathological role of EP4 in various inflammatory diseases. In this study, we investigated the importance of the EP4 receptor, and the efficacy of a selective EP4 agonist to alter hepatic ischemia/reperfusion (I/R) injury, an important cause of damage in liver resection and transplantation. We used an established murine I/R injury model, 70% partial hepatic ischemia for 90 minutes in male C57BL/6 mice. The local expression of EP4 messenger RNA (mRNA) in the naive and the ischemic liver at 2 hours after reperfusion was examined using RT-PCR analysis. Some mice received the EP4 selective agonist during I/R. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured as markers of hepatic injury. EP4 expression in the liver was significantly up-regulated at 2 hours after reperfusion. Furthermore, treatment with EP4 agonist significantly inhibited hepatic injury at 6 hours after reperfusion. Our data suggest an inhibitory role of EP4 PGE(2) receptor in hepatic I/R injury and the therapeutic efficacy of a selective EP4 agonist for liver protection.lld:pubmed
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pubmed-article:15808664pubmed:dateRevised2010-11-18lld:pubmed
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pubmed-article:15808664pubmed:articleTitleRole of EP4 prostaglandin E2 receptor in the ischemic liver.lld:pubmed
pubmed-article:15808664pubmed:affiliationDepartment of Surgery, Nara Medical University School of Medicine, Nara, Japan.lld:pubmed
pubmed-article:15808664pubmed:publicationTypeJournal Articlelld:pubmed
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