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anandamide/turse
Link salvestatakse lõikelauale
Leht 1 alates 16 tulemused
The endocannabinoid arachidonyl ethanolamide (anandamide) increases pulmonary arterial pressure via cyclooxygenase-2 products in isolated rabbit lungs.
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Several cannabinoids elicit systemic vasodilation, mainly via CB1 cannabinoid and vanilloid receptors. However, effects in the pulmonary circulation are unknown. Using the isolated, ventilated, buffer-perfused rabbit lung, we have shown that the endocannabinoids arachidonyl ethanolamide (anandamide)
Neuroprotection by the endogenous cannabinoid anandamide and arvanil against in vivo excitotoxicity in the rat: role of vanilloid receptors and lipoxygenases.
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Type 1 vanilloid receptors (VR1) have been identified recently in the brain, in which they serve as yet primarily undetermined purposes. The endocannabinoid anandamide (AEA) and some of its oxidative metabolites are ligands for VR1, and AEA has been shown to afford protection against ouabain-induced
Evaluation of fatty acid amides in the carrageenan-induced paw edema model.
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While it has long been recognized that Delta(9)-tetrahydrocannabinol (THC), the primary psychoactive constituent of cannabis, and other cannabinoid receptor agonists possess anti-inflammatory properties, their well known CNS effects have dampened enthusiasm for therapeutic development. On the other
Exogenous anandamide protects rat brain against acute neuronal injury in vivo.
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The endocannabinoid anandamide [N-arachidonoylethanolamine (AEA)] is thought to function as an endogenous protective factor of the brain against acute neuronal damage. However, this has never been tested in an in vivo model of acute brain injury. Here, we show in a longitudinal pharmacological
The "dark side" of endocannabinoids: a neurotoxic role for anandamide.
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Endocannabinoids, including 2-arachidonoylglycerol and anandamide (N-arachidonoylethanolamine; AEA), have neuroprotective effects in the brain through actions at CB1 receptors. However, AEA also binds to vanilloid (VR1) receptors and induces cell death in several cell lines. Here we show that
The effects of peptide and lipid endocannabinoids on arthritic pain at the spinal level.
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BACKGROUND
Hemopressin, a nonapeptide (PVNFKFLSH: HP) derived from the α chain of hemoglobin was shown to interact specifically with brain cannabinoid CB(1) receptors. Therefore, it seems to be the only peptide structure with cannabinoid activities. Our goal in this study was to further characterize
Endocannabinoids and neuroprotection.
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Traumatic brain injury (TBI) releases harmful mediators that lead to secondary damage. On the other hand, neuroprotective mediators are also released, and the balance between these classes of mediators determines the final outcome after injury. Recently, it was shown that the endogenous brain
Mice lacking fatty acid amide hydrolase exhibit a cannabinoid receptor-mediated phenotypic hypoalgesia.
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Although the N-arachidonoyl ethanolamine (anandamide) binds to cannabinoid receptors and has been implicated in the suppression of pain, its rapid catabolism in vivo by fatty acid amide hydrolase (FAAH) has presented a challenge in investigating the physiological functions of this endogenous
Mustard vesicants alter expression of the endocannabinoid system in mouse skin.
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Vesicants including sulfur mustard (SM) and nitrogen mustard (NM) are bifunctional alkylating agents that cause skin inflammation, edema and blistering. This is associated with alterations in keratinocyte growth and differentiation. Endogenous cannabinoids, including N-arachidonoylethanolamine
Cannabidiol Ameliorates Monocrotaline-Induced Pulmonary Hypertension in Rats
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Cannabidiol (CBD) is known for its vasorelaxant (including in the human pulmonary artery), anti-proliferative and anti-inflammatory properties. The aim of our study was to examine the potential preventive effect of chronic CBD administration (10 mg/kg/day for three weeks) on monocrotaline
Oral repeated-dose toxicity studies of BIA 10-2474 in cynomolgus monkeys.
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BIA 10-2474 (3-(1-(cyclohexyl(methyl)carbamoyl)-1H-imidazol-4-yl)pyridine 1-oxide) is a novel fatty acid amide hydrolase (FAAH) inhibitor developed by BIAL for the treatment of medical conditions which would benefit from enhanced levels of endogenous anandamide (AEA) such as pain disorders. During a
Oral repeated-dose toxicity studies of BIA 10-2474 in Wistar rat.
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BIA 10-2474 is a novel fatty acid amide hydrolase (FAAH) inhibitor developed for the treatment of medical conditions which would benefit from enhanced levels of endogenous anandamide (AEA) such as pain disorders. During a Phase I clinical trial one subject died after receiving BIA 10-2474 and four
The Endocannabinoid Reuptake Inhibitor WOBE437 Is Orally Bioavailable and Exerts Indirect Polypharmacological Effects via Different Endocannabinoid Receptors.
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Different anandamide (AEA) transport inhibitors show antinociceptive and antiinflammatory effects in vivo, but due to their concomitant inhibition of fatty acid amide hydrolase (FAAH) and overall poor bioavailability, they cannot be used unequivocally to study the particular role of endocannabinoid
Cannabinoids in acute gastric damage and pancreatitis.
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Recent studies have shown that stimulation of cannabinoid 1 (CB1) receptor reduces the area of ischemic myocardial necrosis and affects activity of the digestive tract. The aim of the present study was to check whether the administration of CB1 receptor agonist or antagonist affects the
Cannabinoids reduce hyperalgesia and inflammation via interaction with peripheral CB1 receptors.
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Central antinociceptive effects of cannabinoids have been well documented. However, relatively little is known about the peripheral effects of the cannabinoids on inflammation. In the present study, we evaluated the effects of peripherally administered cannabinoids on three indices of inflammation:
Kõige täiuslikum ravimtaimede andmebaas, mida toetab teadus
- Töötab 55 keeles
- Taimsed ravimid, mida toetab teadus
- Maitsetaimede äratundmine pildi järgi
- Interaktiivne GPS-kaart - märgistage ürdid asukohas (varsti)
- Lugege oma otsinguga seotud teaduspublikatsioone
- Otsige ravimtaimi nende mõju järgi
- Korraldage oma huvisid ja hoidke end kursis uudisteuuringute, kliiniliste uuringute ja patentidega
Sisestage sümptom või haigus ja lugege ravimtaimede kohta, mis võivad aidata, tippige ürdi ja vaadake haigusi ja sümptomeid, mille vastu seda kasutatakse.
* Kogu teave põhineb avaldatud teaduslikel uuringutel
