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Beata Prozorow-Krol,Agnieszka Korolczuk,Grazyna Czechowska,Maria Slomka,Agnieszka Madro,Krzysztof Celinski 대한약학회 2013 Archives of Pharmacal Research Vol.36 No.9
The role of adenosine A3 receptors and theirdistribution in the gastrointestinal tract have been widelyinvestigated. Most of the reports discuss their role inintestinal inflammations. However, the role of adenosineA3 receptor agonist in pancreatitis has not been wellestablished. The aim of this study is (Ed note: Purposestatements should be in present tense) to evaluate theeffects of the adenosine A3 receptor agonist on the courseof sodium taurocholate-induced experimental acute pancreatitis(EAP). The experiments were performed on 80male Wistar rats, 58 of which survived, subdivided into 3groups: C—control rats, I—EAP group, and II—EAPgroup treated with the adenosine A3 receptor agonistIB-MECA (1-deoxy-1-6[[(3-iodophenyl) methyl]amino]-9H-purin-9-yl)-N-methyl-B-D-ribofuronamide at a dose of0.75 mg/kg b.w. i.p. at 48, 24, 12 and 1 h before and 1 hafter the injection of 5 % sodium taurocholate solution intothe biliary–pancreatic duct. Serum for a-amylase and lipasedeterminations and tissue samples for morphologicalexaminations were collected at 2, 6, and 24 h of theexperiment. In the IB-MECA group, a-amylase activitywas decreased with statistically high significance comparedto group I. The activity of lipase was not significantlydifferent among the experimental groups but higher than inthe control group. The administration of IB-MECA attenuatedthe histological parameters of inflammation ascompared to untreated animals. The use of A3 receptoragonist IB-MECA attenuates EAP. Our findings suggestthat stimulation of adenosine A3 receptors plays a positiverole in the sodium taurocholate-induced EAP in rats.