Dipyrone attenuates acute sickness response to lipopolysaccharide in mice

► COX is the key enzyme in the synthesis of PGE. ► LPS induces a collection of physiological and behavioral changes. ► Dipyrone attenuates sickness behavior LPS-induced. Sickness behavior appears to be the expression of a central motivational state that reorganizes the organism's priorities to...

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Published in:Neuroscience letters Vol. 516; no. 1; pp. 114 - 118
Main Authors: Soncini, Roseli, de Souza, Denise F., Neves, Andrea P., Braga, Daniela S., Andrade, Carina A.F., Giusti-Paiva, Alexandre
Format: Journal Article
Language:English
Published: Ireland Elsevier Ireland Ltd 10-05-2012
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Summary:► COX is the key enzyme in the synthesis of PGE. ► LPS induces a collection of physiological and behavioral changes. ► Dipyrone attenuates sickness behavior LPS-induced. Sickness behavior appears to be the expression of a central motivational state that reorganizes the organism's priorities to cope with infectious pathogens. To evaluate the effect of dipyrone in lipopolysaccharide (LPS)-induced sickness behavior, mice were subjected to the forced swim test (FST), tail suspension test (TST), dark–light box test, open field test, sucrose preference intake test and food intake test. LPS administration increased the immobility time in the TST, increased the time spent floating in the FST, and depressed locomotor activity in the open field test. Treatment with LPS decreased the total number of transitions made between the dark and light compartments of the apparatus and induced anhedonia and anorexia. Pre-treatment with dipyrone (10, 50, or 200mg/kg) attenuated behavioral changes induced by LPS in the FST, TST, open field and light–dark box tests. In addition, dipyrone prevented anhedonia and anorexia in mice challenged with LPS. Considering that dipyrone attenuates LPS-induced behavioral changes, it is proposed that LPS-induced sickness behavior is dependent on the COX pathway.
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ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2012.03.070