Reduced mucosal side-effects of acetylsalicylic acid after conjugation with tris-hydroxymethyl-aminomethane. Synthesis and biological evaluation of a new anti-inflammatory compound

Acetylsalicylic acid (ASA) causes adverse haemorrhagic reactions in the upper gastrointestinal (GI) tract, and previous results have suggested that combination therapy with 2-amino-2-(hydroxymethyl)-1,3-propanediol (Tris) could provide protection in this scenario. Based on this hypothesis, our aim...

Teljes leírás

Elmentve itt :
Bibliográfiai részletek
Szerzők: Varga Gabriella
Lajkó Norbert
Ugocsai Melinda
Érces Dániel
Horváth Gyöngyi
Tóth Gábor
Boros Mihály
Ghyczy Miklós
Dokumentumtípus: Cikk
Megjelent: 2016
Sorozat:EUROPEAN JOURNAL OF PHARMACOLOGY 781
doi:10.1016/j.ejphar.2016.04.019

mtmt:3060190
Online Access:http://publicatio.bibl.u-szeged.hu/9454
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520 3 |a Acetylsalicylic acid (ASA) causes adverse haemorrhagic reactions in the upper gastrointestinal (GI) tract, and previous results have suggested that combination therapy with 2-amino-2-(hydroxymethyl)-1,3-propanediol (Tris) could provide protection in this scenario. Based on this hypothesis, our aim was to develop a new compd. from ASA and Tris precursors and to characterize the biol. effects of ASA-Tris and the derivs. ASA-bis- and mono-hydroxymethyl-aminomethane (ASA-Bis, ASA-Mono, resp.) using in vivo and in vitro test systems. ASA or ASA conjugates (0.55 mmol/kg, each) were administered intragastrically to Sprague-Dawley rats. Changes in the mucosal structure and in the serosal microcirculation were detected by in vivo imaging techniques, the plasma TNF-alpha, tissue xanthine oxidoreductase and myeloperoxidase activities, and liver cytochrome c changes were also detd. In two sep. series, platelet aggregation and carrageenan arthritis-induced inflammatory pain were measured in control, ASA and ASA-Tris-treated groups. Severe mucosal injury and a significant decrease in serosal red blood cell velocity developed in the ASA-treated group and an ∼2-fold elevation in proinflammatory mediator levels evolved. ASA-Tris did not cause bleeding, microcirculatory dysfunction, mucosal injury or an elevation in proinflammatory markers. The ASA-Mono and ASA-Bis conjugates did not cause macroscopic bleeding, but the inflammatory activation was apparent. ASA-Tris did not influence the cyclooxygenase-induced platelet aggregation significantly, but the inflammatory pain was reduced as effectively as in the case of equimolar ASA doses. ASA-Tris conjugation is an effective approach through which the GI side-effects of ASA are controlled by decreasing the cytokine-mediated progression of pro-inflammatory events. [on SciFinder(R)] 
700 0 1 |a Lajkó Norbert  |e aut 
700 0 1 |a Ugocsai Melinda  |e aut 
700 0 1 |a Érces Dániel  |e aut 
700 0 1 |a Horváth Gyöngyi  |e aut 
700 0 1 |a Tóth Gábor  |e aut 
700 0 1 |a Boros Mihály  |e aut 
700 0 1 |a Ghyczy Miklós  |e aut 
856 4 0 |u http://publicatio.bibl.u-szeged.hu/9454/1/Varga_EJP_2016_u.pdf  |z Dokumentum-elérés