期刊
NEUROPHARMACOLOGY
卷 54, 期 1, 页码 16-22出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuropharm.2007.05.015
关键词
cannabinoids; lipids; lipase; microglial cells; hydrolysis; NAAA
资金
- NATIONAL INSTITUTE ON DRUG ABUSE [R01DA014486, R21DA022469] Funding Source: NIH RePORTER
- NIDA NIH HHS [DA014486, R01 DA014486-05, R01 DA014486, R21 DA022469, DA022469, R01 DA014486-06A2] Funding Source: Medline
Microglial cell activation and migration play an important role in neuroinflammation propagation. While it is known that the lipid transmitter palmitoylethanolamide (PEA) regulates microglial migration by interacting with a cannabinoid-like receptor, the production and inactivation of this lipid by microglia has never been addressed directly. Here we show that the mouse microglial cell line BV-2 produces and hydrolyzes PEA. The carbamate compound URB602 inhibits PEA hydrolysis in BV-2 cell homogenates and increases PEA levels in intact cells, whereas the FAAH inhibitor URB597 and serine-hydrolase inhibitor MAFP do not affect PEA levels in intact cells. This unique pharmacological profile of inhibitors on PEA hydrolysis suggests the involvement of a previously undescribed enzyme that degrades PEA. This enzyme expressed by microglia constitutes a promising target for controlling the propagation of neuroinflammation. Published by Elsevier Ltd.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据