脂肪酸酰胺水解酶抑制对小脑神经元的细胞活力影响
Cellular viability effects of fatty acid amide hydrolase inhibition on cerebellar neurons.
作者信息
Lueneberg Kathia, Domínguez Guadalupe, Arias-Carrión Oscar, Palomero-Rivero Marcela, Millán-Aldaco Diana, Morán Julio, Drucker-Colín René, Murillo-Rodríguez Eric
机构信息
Department of Neurology, Philipps University, D-35033 Marburg, Germany.
出版信息
Int Arch Med. 2011 Aug 19;4(1):28. doi: 10.1186/1755-7682-4-28.
The endocannabinoid anandamide (ANA) participates in the control of cell death inducing the formation of apoptotic bodies and DNA fragmentation. The aim of this study was to evaluate whether the ANA degrading enzyme, the fatty acid amide hydrolase (FAAH), would induce cellular death. Experiments were performed in cerebellar granule neurons cultured with the FAAH inhibitor, URB597 (25, 50 or 100 nM) as well as endogenous lipids such as oleoylethanolamide (OEA) or palmitoylethanolamide (PEA) and cellular viability was determined by MTT test. Neurons cultured with URB597 (25, 50 or 100 nM) displayed a decrease in cellular viability. In addition, if cultured with OEA (25 nM) or PEA (100 nM), cellular death was found. These results further suggest that URB597, OEA or PEA promote cellular death.
内源性大麻素花生四烯酸乙醇胺（ANA）参与细胞死亡的调控，可诱导凋亡小体的形成和DNA片段化。本研究旨在评估ANA降解酶——脂肪酸酰胺水解酶（FAAH）是否会诱导细胞死亡。实验在培养的小脑颗粒神经元中进行，使用FAAH抑制剂URB597（25、50或100 nM）以及内源性脂质如油酰乙醇胺（OEA）或棕榈酰乙醇胺（PEA），并通过MTT试验测定细胞活力。用URB597（25、50或100 nM）培养的神经元细胞活力下降。此外，若用OEA（25 nM）或PEA（100 nM）培养，会发现细胞死亡。这些结果进一步表明，URB597、OEA或PEA会促进细胞死亡。
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