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Stranica 1 iz 655 rezultatima
Norepinephrine is a more potent inhibitor of tumor necrosis factor over a range of doses than dopamine.
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In the current study, we test the hypothesis that norepinephrine has greater anti-inflammatory effects versus dopamine over a range of doses in a model of lipopolysaccharide (LPS)-stimulated cytokine release in human saphenous vein. Segments of saphenous vein were cut and separated into 1 mm x 1 mm
Phentolamine use in a neonate for the prevention of dermal necrosis caused by dopamine: a case report.
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Skin ischemia, necrosis, and gangrene are uncommon but known complications of dopamine extravasation. In most cases, these complications are associated with the use of high-dosage dopamine infusion. Subcutaneous phentolamine has been used as a therapeutic agent for these complications. However, this
Dopamine increases interleukin 6 release and inhibits tumor necrosis factor release from rat adrenal zona glomerulosa cells in vitro.
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Interleukin 6 (IL-6) and tumor necrosis factor (TNF) are released from the zona glomerulosa of rat adrenal glands. The release of these cytokines from adrenal cells is regulated by interleukin 1 beta (IL-1 beta) and lipopolysaccharide (LPS), which are involved in the immune and inflammatory
Dopamine protects cerebral autoregulation and prevents hippocampal necrosis after traumatic brain injury via block of ERK MAPK in juvenile pigs.
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Traumatic brain injury (TBI) contributes to morbidity in children, and more boys experience TBI. Cerebral autoregulation is impaired after TBI, contributing to poor outcome. Cerebral Perfusion Pressure (CPP) is often normalized by use of vasoactive agents to increase mean arterial pressure (MAP). In
Lipopolysaccharide (LPS)-induced dopamine cell loss in culture: roles of tumor necrosis factor-alpha, interleukin-1beta, and nitric oxide.
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Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopamine (DA) neurons of the substantia nigra pars compacta (SNc). Although the exact mechanisms responsible for this cell loss are unclear, emerging evidence suggests the involvement of inflammatory events. In the
Tumor necrosis factor alpha is toxic to embryonic mesencephalic dopamine neurons.
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Levels of the proinflammatory cytokine tumor necrosis factor alpha (TNFalpha) are increased in postmortem brain and cerebral spinal fluid from patients with Parkinson's disease (PD). This observation provides a basis for associating TNFalpha with neurodegeneration, but a specific toxicity in
Changes in AMPA glutamate and dopamine D2 receptors in hypoxic-ischemic basal ganglia necrosis.
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Changes in the AMPA glutamate receptor subunits (GluR1, 2-3, and 4) and dopamine D2 receptor (D2R) were investigated in 16 cases of hypoxic-ischemic basal ganglia necrosis (BGN) by immunohistochemistry. Immunoreactivity to GluR1, 2-3, and 4 was observed in the cytoplasm and dendrites of small and
Intra-parenchymal injection of tumor necrosis factor-alpha and interleukin 1-beta produces dopamine neuron loss in the rat.
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Inflammatory processes are thought to underlie the dopamine (DA) neuron loss seen in Parkinson's disease (PD). However, it is not known if the inflammation precedes that loss, or is a consequence of it. We injected tumor necrosis factor alpha (TNFalpha) and interleukin 1 beta (IL-1beta) into the
Effect of methyl derivatives of dopamine on tumor necrosis factor alpha and lipid peroxidation.
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We recently demonstrated that melatonin, N-acetylserotonin (NAS), and N-acetyldopamine (NAD) attenuate the synthesis of lipopolysaccharide (LPS)-stimulated tumor necrosis factor-alpha (TNF-alpha) and the generation of oxidant radicals. In this study, we examined whether acetyl and methyl derivatives
Neuropathological characteristics and alteration of the dopamine D2 receptor in hypoxic-ischemic basal ganglia necrosis.
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The neuropathological characteristics and alteration of the dopamine D2 receptor (D2R) were investigated in 27 cases of hypoxic-ischemic basal ganglia necrosis (BGN) by means of neuropathological and immunohistochemical methods. Perinatal hypoxic-ischemic BGN manifested neuronal karyorrhexis as well
Modulation of lipopolysaccharide-induced tumor necrosis factor-alpha and nitric oxide production by dopamine receptor agonists and antagonists in mice.
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The effects of various agonist and antagonists of dopamine D1 and D2 receptors on lipopolysaccharide (LPS)-induced tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) production was investigated in mice. Pretreatment of animals with bromocryptine or quinpirole, agonists of dopamine D2
A novel molecule 'shati' increases dopamine uptake via the induction of tumor necrosis factor-alpha in pheochromocytoma-12 cells.
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The psychostimulant properties of methamphetamine (METH) are associated with an increase in extracellular dopamine (DA) levels in the brain, via facilitation of DA's release from pre-synaptic nerve terminals and inhibition of its reuptake through DA transporter. Recently, we have demonstrated that
Sepsis-induced changes in behavioral stereotypy in rats; involvement of tumor necrosis factor-alpha, oxidative stress, and dopamine turnover.
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BACKGROUND
Sepsis-associated encephalopathy (SAE) is defined as a diffuse or multifocal cerebral dysfunction that generally occurs early during severe sepsis. The complete pathophysiology of SAE is unknown, but several mechanisms including endotoxins, inflammatory mediators, the alteration of amino
Antioxidants inhibit the human cortical neuron apoptosis induced by hydrogen peroxide, tumor necrosis factor alpha, dopamine and beta-amyloid peptide 1-42.
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Several substances related to the neurodegenerative diseases of Alzheimer and Parkinson, such as hydrogen peroxide, tumor necrosis factor alpha, dopamine and beta-amyloid peptide 1-42, have been shown to induce apoptosis in tumoral cell lines and rat neurons but not in human neurons. Moreover, the
Attenuation of oxidative neuronal necrosis by a dopamine D1 agonist in mouse cortical cell cultures.
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Events which lead to an increase in intracellular free radicals induce necrotic cell death of cultured cortical neurons. In the present study, we report that treatment with 1 microM (+/-)-SKF-38393 hydrochloride, a selective D1 agonist, as well as 100 microM trolox, a lipophilic vitamin E analogue,
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