n-stearoyltyrosine has been researched along with anandamide* in 2 studies
2 other study(ies) available for n-stearoyltyrosine and anandamide
| Article | Year |
|---|---|
N-stearoyltyrosine protects primary cortical neurons against oxygen-glucose deprivation-induced apoptosis through inhibiting anandamide inactivation system.
N-stearoylthrosine (NST), a synthesized anandamide (AEA) analogue, plays a neuroprotective role in neurodegenerative diseases and cerebrovascular diseases. Several studies have demonstrated that the endocannabinoids systems (ECS) are involved in the neuroprotective effects against cerebral ischemic injury. Oxygen-glucose deprivation (OGD)-induced neuronal injury elevated the levels of endocannabinoids and activated ECS. This research was conducted to investigate the neuroprotective effect of NST against OGD-induced neuronal injury in cultured primary cortical neurons and the potential mechanism involved. Cortical neurons were treated with NST at indicate concentrations for 30min prior to injury and OGD injured neurons were incubated with normal conditions for 0-24h. The best neuroprotective effect of NST against OGD-induced injury occurred at 10μM. All data indicated that the neuroprotective effect of NST against OGD-induced injury resulted from blocking anandamide membrane transporter (AMT) (IC Topics: Amidohydrolases; Animals; Apoptosis; Arachidonic Acids; bcl-2-Associated X Protein; Cell Hypoxia; Cell Survival; Cells, Cultured; Cerebral Cortex; Embryo, Mammalian; Endocannabinoids; Enzyme Inhibitors; Gene Expression Regulation; Glucose; L-Lactate Dehydrogenase; Neurons; Nitric Oxide; Oxygen; Polyunsaturated Alkamides; Rats; Rats, Sprague-Dawley; Tyrosine | 2017 |
N-Stearoyltyrosine protects primary cortical neurons against Aβ(1-40)-induced injury through inhibiting endocannabinoid degradation.
N-stearoyltyrosine (NsTyr) as an anandamide (AEA) analog has close relationships with AEA not only in structure but also in terms of biological actions of endocannabinoids. Since β-amyloid (Aβ)-induced primary neuronal injury involves the activation of the endocannabinoid systems (ECS), the protective effects of NsTyr against Aβ(1-40)-induced neuronal injury and the mechanism were studied systematically in this paper.. Cortical neurons were incubated with Aβ(1-40) for 24 h. NsTyr was added to indicated concentrations 30 min prior to injury.. The best effects of NsTyr on Aβ(1-40)-induced primary neuronal injury occurred at 10 μM. The mechanism of NsTyr on neuroprotective effects against Aβ(1-40)-induced cellular death first involved anti-apoptosis resulting from the activation of cannabinoid receptors, then the pre-receptor regulation of AEA by the inhibition of endocannabinoid inactivation. These data demonstrated that the protective effects of NsTyr on Aβ(1-40)-induced primary neuronal injury resulted from the inhibition of fatty acid amide hydrolase (FAAH) (IC50=16.54 nM) and blocked AEA uptake mediated by anandamide membrane transporter (AMT) (IC50=11.74 nM).. The activation of ECS by inhibiting the degradation of AEA is an effective pharmacological approach to suppress Aβ-induced neuropathic injury. Our research could result in a more realistic alternative for AD treatment. Topics: Amidohydrolases; Amyloid beta-Peptides; Animals; Apoptosis; Arachidonic Acids; Cerebral Cortex; Dose-Response Relationship, Drug; Endocannabinoids; Inhibitory Concentration 50; Membrane Transport Proteins; Neurons; Neuroprotective Agents; Peptide Fragments; Polyunsaturated Alkamides; Rats; Rats, Sprague-Dawley; Receptors, Cannabinoid; Tyrosine | 2015 |