期刊
NEUROSCIENCE LETTERS
卷 470, 期 1, 页码 33-37出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2009.12.050
关键词
Aspirin-triggered lipoxin; 15-Epi-lipoxin A(4); Endocannabinoid; Anandamide; Lipoxygenase
资金
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq-Brazil)
Evidence are that inhibition of cyclooxygenase 2 (COX-2) enhances endocannabinoid signaling, indicating a crosstalk between these two eicosanoid pathways. Aspirin, a non-selective COX inhibitor, acetylates COX-2 with generation of a lipoxygenase (LOX) substrate, whose end product is the 15-epi-lipoxin A(4) (15-epi-LXA(4)), an aspirin-triggered lipoxin. Our objective was to investigate whether 15-epi-LXA(4) would potentiate in vivo effects of the endocannabinoid anandamide (AEA). Catalepsy was selected as a behavioral parameter and tested 5 min after AEA injection in all experiments. AEA induced close-dependent (200 pmol/2 mu l, i.c.v.) catalepsy. A sub-dose of AEA (110 pmol/2 mu l, i.c.v.) was potentiated by aspirin (300 mg/kg, p.o.) via a 5-LOX-dependent step. The cataleptic effect induced by the interaction between sub-doses of 1 5-epi-LXA(4) (0.01 pmol/2 mu l, i.c.v.) and AEA (10 pmol/2 mu l, i.c.v.) was prevented by the cannabinoid CB1 receptors antagonist SR141716A (1 mg/kg, i.p.), but not by the antagonist of lipoxin ALX receptors Boc-2 (10 mu g/kg, i.p.). While previous studies have shown that COX inhibition itself may enhance endocannabinoid effects, here we add another piece of evidence revealing that a LOX-derivative produced in consequence of COX-2 acetylation participates in this process. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
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