Palmidrol是一种内源性脂肪酸酰胺，可预防呼吸道病毒感染。

Palmitoylethanolamide(PEA) , an endogenous fatty acid amide, activates PPAR-α selectively in vitro (EC50=3.1±0.4 μM）.

PEA protects cultured mouse cerebellar granule cells from glutamate toxicity and enhances microglial cell motility. In the mitochondrial fraction from cells stimulated with PEA, steroidogenic acute regulatory protein (StAR) and cytochrome P450 enzyme(P450scc) expression increases, both comprising proteins considered to be involved in crucial steps of neurosteroid formation. Moreover, PEA shows a protective effect, reducing malondialdehyde formation in cells treated with L-buthionine-(S,R)-sulfoximine, a glutathione depletor and the effect of PEA is partially inhibited by finasteride, a 5a-reductase inhibitor[2].

PEA attenuates inflammation in wild-type mice but has no effect in mice deficient in PPAR-α. PEA has been shown to inhibit peripheral inflammation and mast-cell degranulation as well as to exert neuroprotective and antinociceptive effects in rats and mice. These actions are accompanied by changes in nitric oxide production, neutrophil influx, and expression of proinflammatory proteins such as inducible nitric oxide synthase and cyclooxygenase-2[1]. In addition to its known anti-inflammatory activity, PEA regulates many pathophysiological processes, including pain perception, convulsions, and neurotoxicity. In the central nervous system (CNS), where PEA is present at detectable levels, its concentrations significantly increase under pathological conditions, such as excitotoxicity, brain ischaemia and neuroinflammation[2].

C6 glioma cells (300 000?P60 dish) or astrocyte primary culture are incubated in serum-free DMEM at 37℃ for at least 24 h before each experiment. Then, cells are treated with PEA (10 μM) for 24 h in serum-free medium, in the presence and absence of GW6471 (10 μM) added 30 min before ethanolamide treatment. The concentration of PEA is chosen on the basis of preliminary experiments, assessing drug efficacy without modifi-cation of cell viability. PEA and GW6471 are first dissolved in absolute ethanol and then diluted with DMEM. The final ethanol concentration was< 0.5%. Mitochondrial protein extracts from C6 or astrocytes are obtained. Alternatively after 24 h of starvation in serum-free DMEM, C6 cells are treated with FIN (100 nM). After 30 min, PEA (10 μM) and?or ALLO (3 μM) is added and, 30 min later, are stimulated with BSO (10 mM). After 18 h, MDA is evaluated. In this set of experiments, FIN and?or PEA are dissolved in dimethylsulphoxide (DMSO) and then diluted with DMEM (0.1% final DMSO concentration).(Only for Reference)

544-31-0

C18H37NO2

299.499

N-palmitoylethanolamine;Mackpeart DR 14V;Impulsin;Palmidrol;帕米醇;Loramine P 256;AM 3112

DMSO:6 mg/mL (20 mM)
Ethanol:7.5 mg/mL (25 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years