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anandamide/некроза
Веза се чува у привремену меморију
Страна 1 од 78 резултати
Anandamide induces necrosis in primary hepatic stellate cells.
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The endogenous cannabinoid anandamide (AEA) is a lipid mediator that blocks proliferation and induces apoptosis in many cell types. Although AEA levels are elevated in liver fibrosis, its role in fibrogenesis remains unclear. This study investigated effects of AEA in primary hepatic stellate cells
Effects of tumour necrosis factor α upon the metabolism of the endocannabinoid anandamide in prostate cancer cells.
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Tumour necrosis factor α (TNFα) is involved in the pathogenesis of prostate cancer, a disease where disturbances in the endocannabinoid system are seen. In the present study we have investigated whether treatment of DU145 human prostate cancer cells affects anandamide (AEA) catabolic pathways.
Inhibition of hepatic tumour necrosis factor-alpha attenuates the anandamide-induced vasoconstrictive response in cirrhotic rat livers.
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BACKGROUND
Increased anandamide, an endocannabinoid that interacts with both cannabinoid CB(1) and CB(2) receptors, can induce hepatic vasoconstrictive responses that contribute to the increased intrahepatic resistance (IHR) in cirrhotic rats. Chronic endotoxaemia and the subsequent release of
Anandamide inhibits macrophage-mediated killing of tumor necrosis factor-sensitive cells.
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Anandamide (arachidonoylethanolamide) was shown to inhibit macrophage-mediated killing of tumor necrosis factor-sensitive murine L929 fibroblasts. Scanning electron microscopy (SEM) demonstrated that L929 cells, co-cultured with Propionibacterium acnes (P. acnes)-activated peritoneal macrophages
Decidual NK cell-derived conditioned medium from miscarriages affects endometrial stromal cell decidualisation: endocannabinoid anandamide and tumour necrosis factor-α crosstalk.
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Lipopolysaccharide-induced pulmonary inflammation is not accompanied by a release of anandamide into the lavage fluid or a down-regulation of the activity of fatty acid amide hydrolase.
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The effect of lipopolysaccharide inhalation upon lung anandamide levels, anandamide synthetic enzymes and fatty acid amide hydrolase has been investigated. Lipopolysaccharide exposure produced a dramatic extravasation of neutrophils and release of tumour necrosis factor alpha into the
Endogenous cannabinoid anandamide impairs cell growth and induces apoptosis in chondrocytes.
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Endocannabinoids has been described to be involved in articular degenerative disease by modulating nociception and immune system. However, the role of the endocannabinoid anandamide on chondrocyte cell viability is still unclear. Therefore, we decided to study anandamide's effects on chondrocytes
Accumulation of the anandamide precursor and other N-acylethanolamine phospholipids in infant rat models of in vivo necrotic and apoptotic neuronal death.
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It has been demonstrated that the endogenous cannabinoid receptor ligand, anandamide, and other N-acylethanolamines (NAEs), accumulate during neuronal injury in vitro, a process that may be linked to the neuroprotective effects of NAEs. The crucial step for generation of NAEs is the synthesis of the
[Effects of anandamide on the activation and proliferation of hepatic stellate cells through cannabinoid-2 receptors].
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OBJECTIVE
To study the effects of endogenous cannabinoid anandamide (AEA) and its putative endocannabinoid receptors (CBR) on the activation and proliferation of hepatic stellate cells (HSC) and to study the role played by AEA during liver fibrosis.
METHODS
By using immunofluorescence and cell
High levels of anandamide, an endogenous cannabinoid, block the growth of sheep preimplantation embryos by inducing apoptosis and reversible arrest of cell proliferation.
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BACKGROUND
The process of implantation is mediated by various molecules, one of which is anandamide (AEA), a lipid signalling ligand belonging to the family of endocannabinoids. AEA exerts its effects on implantation by binding to the Type 1 Cannabinoid Receptor (CB1-R), expressed in both
Characterisation of the prostaglandin E2-ethanolamide suppression of tumour necrosis factor-α production in human monocytic cells.
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OBJECTIVE
Prostaglandin ethanolamides or prostamides are naturally occurring neutral lipid derivatives of prostaglandins that have been shown to be synthesised in vivo following COX-facilitated oxygenation of arachidonoyl ethanolamine (anandamide). Although the actions of prostaglandins have been
The hypothalamic endocannabinoid system participates in the secretion of oxytocin and tumor necrosis factor-alpha induced by lipopolysaccharide.
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This study investigated the participation of the hypothalamic endocannabinoid system in the response to lipopolysaccharide (LPS) challenge evaluating oxytocin (OXT) and tumor necrosis factor-alpha (TNF-alpha) plasma levels in vivo and their release from hypothalamic fragments in vitro. LPS increased
[Membrane cholesterol mediates the endocannabinoids-anandamide affection on HepG2 cells].
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OBJECTIVE
To study the effect of anandamide (AEA) on necrosis in HepG2 cells and to explore the role of AEA in progression of liver cancer.
METHODS
Localization of the fatty acid hydrolytic enzyme (FAAH), cannabinoid receptors 1(CB1) and cannabinoid receptors 2 (CB2) proteins was detected in L02 and
Anandamide induces cell death through lipid rafts in hepatic stellate cells.
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OBJECTIVE
Anandamide (AEA), the most extensively studied endocannabinoid, and its putative cannabinoid receptors, CB1 and CB2, exert a variety of physiological and pharmacological effects in chronic liver diseases, such as hyperdynamic circulation. Anandamide selectively blocks proliferation and
Anandamide inhibits nuclear factor-kappaB activation through a cannabinoid receptor-independent pathway.
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Anandamide (arachidonoylethanolamine, AEA), an endogenous agonist for both the cannabinoid CB(1) receptor and the vanilloid VR1 receptor, elicits neurobehavioral, anti-inflammatory, immunomodulatory, and proapoptotic effects. Because of the central role of nuclear factor-kappaB (NF-kappaB) in the
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