Inhibition of microglial fatty acid amide hydrolase modulates LPS stimulated release of inflammatory mediators
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چکیده
منابع مشابه
Regulation of inflammatory pain by inhibition of fatty acid amide hydrolase.
Although cannabinoids are efficacious in laboratory animal models of inflammatory pain, their established cannabimimetic actions diminish enthusiasm for their therapeutic development. Conversely, fatty acid amide hydrolase (FAAH), the chief catabolic enzyme regulating the endogenous cannabinoid N-arachidonoylethanolamine (anandamide), has emerged as an attractive target for treating pain and ot...
متن کاملFatty acid amide hydrolase substrate specificity.
Fatty acid amide hydrolase (FAAH), also referred to as oleamide hydrolase and anandamide amidohydrolase, is a serine hydrolase responsible for the degradation of endogenous oleamide and anandamide, fatty acid amides that function as chemical messengers. FAAH hydrolyzes a range of fatty acid amides, and the present study examines the relative rates of hydrolysis of a variety of natural and unnat...
متن کاملEpigenetic Regulation of Fatty Acid Amide Hydrolase in Alzheimer Disease
OBJECTIVE Alzheimer disease (AD) is a progressive, degenerative and irreversible neurological disorder with few therapies available. In search for new potential targets, increasing evidence suggests a role for the endocannabinoid system (ECS) in the regulation of neurodegenerative processes. METHODS We have studied the gene expression status and the epigenetic regulation of ECS components in ...
متن کاملStructure and function of fatty acid amide hydrolase.
Fatty acid amide hydrolase (FAAH) is a mammalian integral membrane enzyme that degrades the fatty acid amide family of endogenous signaling lipids, which includes the endogenous cannabinoid anandamide and the sleep-inducing substance oleamide. FAAH belongs to a large and diverse class of enzymes referred to as the amidase signature (AS) family. Investigations into the structure and function of ...
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ژورنال
عنوان ژورنال: FEBS Letters
سال: 2007
ISSN: 0014-5793
DOI: 10.1016/j.febslet.2007.05.037