Journal: Neuroscience letters

Article Title: Aspirin-triggered lipoxin induces CB1-dependent catalepsy in mice.

doi: 10.1016/j.neulet.2009.12.050

Figure Lengend Snippet: Fig. 1. Schematic representation of the eicosanoid metabolic pathways, including the sites of action of the substances used in the present study. Arachidonic acid is the common precursor of prostaglandins and other prostanoids, endocannabinoids, leukotriens and lipoxins. From left to right: the leukotriens and lipoxins share a common metabolic pathway using lipoxygenases (LOX) to generate the 15-HPETE precursor. Then, leukotriene hydrolase yields the leukotriens, which act on leukotriene receptors (CysLT, BLT). Lipoxins are primarily generated via a serial LOX pathway and act at ALX receptors (specially lipoxin A4, LXA4), previously named formyl peptide-like receptors 1 (FPRL-1). An alternative route for the synthesis of 15-epi-lipoxin A4 (15-epi-LXA4) is via acetylation of cyclooxygenase (COX) 2 by aspirin. (For this reason 15-epi-LXA4 is named aspirin-triggered lipoxin, or ATL.) Prostaglandins are synthesized by COX 1/2 enzymes and act at the level of prostaglandin receptors (PGD, PGE, PGI, PGF). Endocannabinoids are synthesized either via phospholipase D (PLD) for anandamide (AEA) or via diacylglycerol lipase (DAGL) for 2-araquidonoyl glycerol (not represented) and activate CB1/CB2 receptors. Aspirin inhibits COX enzymes and acetylate COX-2; MK-886 inhibits the LOX pathway; SR141716A is an antagonist of CB1 receptors; BOC-2 is an antagonist of ALX receptors. All these drugs have been used in the present study. Dashed line represents synthetic route. Solid line represents site of action.

Article Snippet: Anandamide (TOCRIS, USA) and 15-epi-lipoxin A4 (Oxford iomedical Research, USA) were dissolved in 0.1 M phosphateuffered saline (PBS), with final ethanol concentration of 0.5% and njected via i.c.v. route.

Techniques: Generated, Synthesized

Journal: Neuroscience letters

Article Title: Aspirin-triggered lipoxin induces CB1-dependent catalepsy in mice.

doi: 10.1016/j.neulet.2009.12.050

Figure Lengend Snippet: Fig. 2. (A) Anandamide (AEA) induces dose-dependent (10–200 pmol/2 l, i.c.v.) catalepsy compared to control (C; 0.5% ethanol). (B and C) Aspirin (300 mg/kg, p.o.) potentiates the effects of a sub-dose of AEA (10 pmol/2 l, i.c.v.). (D) The 5-lipoxygenase inhibitor MK-886 (1 mg/kg, i.p.) prevents the aspirin-induced potentiation of AEA effects (n = 6–8 animals per group) ***p < 0.001 compared to control ###p < 0.001 compared to the combined treatment with AEA + aspirin (Duncan’s post hoc test).

Article Snippet: Anandamide (TOCRIS, USA) and 15-epi-lipoxin A4 (Oxford iomedical Research, USA) were dissolved in 0.1 M phosphateuffered saline (PBS), with final ethanol concentration of 0.5% and njected via i.c.v. route.

Techniques: Control