Q2. What are the future works mentioned in the paper "The search for the palmitoylethanolamide receptor" ?
These possibilities remain, however, to be explored. As these questions are progressively answered, the authors may not only gain insights on the PEA signaling system, but also identify new potential targets for analgesic and anti-inflammatory medicines.
Q3. What is the role of PPAR-a in the anti-inflammatory action of PEA?
In addition, PPAR-a activators have been shown to inhibit monocyte differentiation and neutrophil function, including endothelial extravasation.
Q4. What is the role of PEA in neuroprotective actions?
Because PEA-induced analgesia is rapid and precedes the compound’s anti-inflammatory actions, it has been suggested that PEA may function as an endogenous regulator ofnociception (Calignano et al., 1998).
Q5. What is the role of FAAH in the synthesis of PEA?
a membrane-bound intracellular serine hydrolase, for which PEA is an excellent substrate(Désarnaud et al., 1995; Hillard et al., 1995; Ueda et al., 1995), is present in all mammalian tissues, but isparticularly abundant in brain and liver (Cravatt and Lichtman, 2002).
Q6. What is the effect of phorbol esters on PEA levels in mice?
The authors found that phorbol esters/protein kinase C activators thatexert profound proinflammatory effects decrease PEA levels in mouse abdominal skin.
Q7. What is the role of cannabinoid receptors in marijuana?
Cannabinoid receptors, the molecular targets of the psychoactive component in marijuana, delta-9-tetrahydrocannabinol (THC), belong to the G-protein-coupled receptor super family (Matsuda et al.,1990; Munro et al., 1993).
Q8. What caused arenewal of interest in PEA?
It was the discovery that another fatty acid amide, anandamide (arachidonoy-lethanolamide), is an endogenous agonist for cannabinoid receptors (Devane et al., 1992) that caused arenewal of interest in PEA.
Q9. What is the effect of PEA on breast cancer?
Di Marzo et al. (2001) suggested that in human breast cancer cells, PEAmay work by inhibiting FAAH expression, which should lead to an increase in anandamide levels.
Q10. What is the mechanism of synthesis of PEA?
Isolated cells,including brain neurons, macrophages (J774), basophils (RBL-2H3), and neuroblastoma (N18TG2) cells, have also been reported to generate PEA in response to ionomycin or digestion with exogenous PLD(Bisogno et al., 1997; Cadas et al., 1997; Di Marzo et al., 1994).
Q11. What is the role of PPAR-a in the inflammatory process?
A finalquestion is whether non-cannabinoid FAEs, such as stearoylethanolamide (Maccarrone et al., 2002; Terrazzino et al., 2004), also activate PPAR-a or related transcription factors.
Q12. What is the role of SR144528 in the regulation of PEA?
Adding to the PEA mystery, the CB2 antagonist/inverse agonist SR144528 inhibits many, but not all, of the pharmacological actions of PEA(Calignano et al., 1998, 2001; Conti et al., 2002; Jaggar et al., 1998).
Q13. What was the first study on PEA?
The years following the discovery of PEA’s anti-inflammatory effects (Benvenuti et al., 1968;Perlik et al., 1971) witnessed a series of interesting clinical studies on this compound, which wastested under the trade name of Impulsin by the Czech pharmaceutical company, SPOFA.