Role of endogenous adenosine in the acute and late response to allergen challenge in actively sensitized Brown Norway rats

Ellis, K M; Mazzoni, Lazzaro; Fozard, John R.

doi:10.1038/sj.bjp.0705355

Cited by 6 publications

(3 citation statements)

References 37 publications

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“…A reference in vivo dose of EHNA (30 mol/kg) was selected on the basis of a previous study evaluating the anti-inflammatory effects of this drug in a rat model of asthma (Ellis et al, 2003). Effective doses of APP and EHNA were then selected by preliminary experiments designed to assay increasing doses of these compounds (APP, 5, 15, and 45 mol/kg; EHNA, 10, 30, and 90 mol/kg) on food intake, body weight, spleen weight, and macroscopic score in the model of DNBSinduced colitis.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of Adenosine Deaminase Attenuates Inflammation in Experimental Colitis

Antonioli¹,

Fornai²,

Colucci³

et al. 2007

J Pharmacol Exp Ther

104

114

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Adenosine modulates the immune system and inhibits inflammation via reduction of cytokine biosynthesis and neutrophil functions. Drugs able to prevent adenosine catabolism could represent an innovative strategy to treat inflammatory bowel disorders. In this study, the effects of 4-amino-2-(2-hydroxy-1-decyl)pyrazole [3,4-d]pyrimidine (APP; novel adenosine deaminase inhibitor), erythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride (EHNA; standard adenosine deaminase inhibitor), and dexamethasone were tested in rats with colitis induced by 2,4-dinitrobenzenesulfonic acid (DNBS). DNBS-treated animals received APP (5, 15, or 45 mol/kg), EHNA (10, 30, or 90 mol/kg), or dexamethasone (0.25 mol/kg) i.p. for 7 days starting 1 day before colitis induction. DNBS caused bowel inflammation associated with decrease in food intake and body weight. Animals treated with APP or EHNA, but not dexamethasone, displayed greater food intake and weight gain than inflamed rats. Colitis induced increment in spleen weight, which was counteracted by all test drugs. DNBS administration was followed by macroscopic and microscopic inflammatory colonic alterations, which were ameliorated by APP, EHNA, or dexamethasone. In DNBS-treated rats, colonic myeloperoxidase, malondialdehyde, and tumor necrosis factor (TNF)-␣ levels as well as plasma TNF-␣ and interleukin-6 were increased. All test drugs lowered these phlogistic indexes. Inflamed colonic tissues displayed an increment of inducible nitric-oxide synthase mRNA, which was unaffected by APP or EHNA, but reduced by dexamethasone. Cyclooxygenase-2 expression was unaffected by DNBS or test drugs. These findings indicate that 1) inhibition of adenosine deaminase results in a significant attenuation of intestinal inflammation and 2) the novel compound APP is more effective than EHNA in reducing systemic and intestinal inflammatory alterations.

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Section: Methodsmentioning

confidence: 99%

Inhibition of Adenosine Deaminase Attenuates Inflammation in Experimental Colitis

Antonioli¹,

Fornai²,

Colucci³

et al. 2007

J Pharmacol Exp Ther

104

114

View full text Add to dashboard Cite

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“…[12] After pretreatment with EHNA and NBTI, 5% dextrose (0.05 mL/kg/min) was infused for 60 minutes. This group was designed to determine the increase in adenosine availability…”

Section: Methodsmentioning

confidence: 99%

“…[12] After the pretreatment with EHNA and NBTI, citalopram (4 mg/kg/min) was infused during 60 minutes.…”

Section: Methodsmentioning

confidence: 99%

The role of adenosine receptors and endogenous adenosine in citalopram-induced cardiovascular toxicity

et al. 2014

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Aim:We investigated the role of adenosine in citalopram-induced cardiotoxicity.Materials and Methods:Protocol 1: Rats were randomized into four groups. Sodium cromoglycate was administered to rats. Citalopram was infused after the 5% dextrose, 8-Cyclopentyl-1,3-dipropylxanthine (DPCPX; A1 receptor antagonist), 8-(-3-chlorostyryl)-caffeine (CSC; A2a receptor antagonist), or dimethyl sulfoxide (DMSO) administrations. Protocol 2: First group received 5% dextrose intraperitoneally 1 hour prior to citalopram. Other rats were pretreated with erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA; inhibitor of adenosine deaminase) and S-(4-Nitrobenzyl)-6-thioinosine (NBTI; inhibitor of facilitated adenosine transport). After pretreatment, group 2 received 5% dextrose and group 3 received citalopram. Adenosine concentrations, mean arterial pressure (MAP), heart rate (HR), QRS duration and QT interval were evaluated.Results:In the dextrose group, citalopram infusion caused a significant decrease in MAP and HR and caused a significant prolongation in QRS and QT. DPCPX infusion significantly prevented the prolongation of the QT interval when compared to control. In the second protocol, citalopram infusion did not cause a significant change in plasma adenosine concentrations, but a significant increase observed in EHNA/NBTI groups. In EHNA/NBTI groups, citalopram-induced MAP and HR reductions, QRS and QT prolongations were more significant than the dextrose group.Conclusions:Citalopram may lead to QT prolongation by stimulating adenosine A1 receptors without affecting the release of adenosine.

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Biphasic airway–lung response to anaphylactic shock in Brown Norway rats

Barthel

Zheng

Demoulin

et al. 2013

Respiratory Physiology & Neurobiology

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Role of endogenous adenosine in the acute and late response to allergen challenge in actively sensitized Brown Norway rats

Cited by 6 publications

References 37 publications

Inhibition of Adenosine Deaminase Attenuates Inflammation in Experimental Colitis

Inhibition of Adenosine Deaminase Attenuates Inflammation in Experimental Colitis

The role of adenosine receptors and endogenous adenosine in citalopram-induced cardiovascular toxicity

Biphasic airway–lung response to anaphylactic shock in Brown Norway rats

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