Quantitative analysis of cyclooxygenase gene expression on acute gastric injury induced by ischemia-reperfusion in rats

The rat model of acute gastric damage induced by ischemia-reperfusion (I-R) has been used to evaluate the protective effect of various drugs on gastric injury. However, the quantitative expression state of cyclooxygenase (COX) is still unknown in acute gastric injury induced by I-R. Therefore, we ha...

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Bibliographic Details
Published inJapanese Journal of Pharmacology Vol. 73; no. suppl.1; p. 218
Main Authors Kishimoto, Yosuke, Wada, Koujchirou, Nakamoto, Kentaro, Ashida, Kumiyo, Kamisaki, Yoshinori, Kawasaki, Hironaka, Itoh, Tadao
Format Journal Article
LanguageEnglish
Published The Japanese Pharmacological Society 1997
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Summary:The rat model of acute gastric damage induced by ischemia-reperfusion (I-R) has been used to evaluate the protective effect of various drugs on gastric injury. However, the quantitative expression state of cyclooxygenase (COX) is still unknown in acute gastric injury induced by I-R. Therefore, we have quantitatively investigated the levels of expression of COX-1 and -2 mRNA in injured gastric tissue using the reverse transcription-competitive polymerase chain reaction method. The mRNA for COX-2 was expressed at low or undetectable levels in the normal gastric tissues in control rats, which were without I-R. The mRNA levels of COX-2 in injured gastric tissues were higher than those in control tissues between 6 hrs and 48 hrs after I-R. The maximum expression of COX-2 mRNA was recorded at 24 hrs (approximately a 200-fold increase). There was a tendency toward an increased level of COX-1 message at the healing stage of gastric damage. The measurement of expression states of COX-1 and -2 mRNA, which have been ascertained in this study, should be useful in understanding in greater detail the roles of COX and prostaglandins in acute gastric disorders, and having a greater appreciation of the etiology of the therapeutic effects of some drugs.
ISSN:0021-5198
1347-3506
DOI:10.1016/S0021-5198(19)45372-9