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Seite 1 von 270 Ergebnisse
Effect of morphine on lipopolysaccharide-induced tumor necrosis factor-alpha production in vivo: involvement of the sympathetic nervous system.
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Morphine treatment modulates a variety of immunological parameters, including tumor necrosis factor-alpha (TNF-alpha) production by activated macrophages in vitro. The aim of our study was to clarify the effect of morphine on lipopolysaccharide (LPS)-induced TNF-alpha production in vivo. Plasma
[Effects of epidurally administration of morphine at thoracic level on expression of tumor necrosis factor-alpha in the lungs in acute myocardial ischemia in rats].
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OBJECTIVE
To investigate the expression of tumor necrosis factor-alpha (TNF-alpha) in lungs following coronary artery occlusion (CAO) and the effect of morphine pretreatment via epidural administration on its expression in the rats.
METHODS
Eighteen adult healthy male Sprague-Dawley (SD) rats were
Priming effect of morphine on the production of tumor necrosis factor-alpha by microglia: implications in respiratory burst activity and human immunodeficiency virus-1 expression.
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Opiates alter a variety of functional activities of the somatic immune system; within the central nervous system, however, their effects on immune responses are unknown. In the present study, we investigated the effect of morphine on the release of tumor necrosis factor (TNF)-alpha from murine
Intermitted pharmacologic pretreatment by xenon, isoflurane, nitrous oxide, and the opioid morphine prevents tumor necrosis factor alpha-induced adhesion molecule expression in human umbilical vein endothelial cells.
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BACKGROUND
The barrier properties of the endothelium are of critical importance during pathophysiologic processes. These barrier properties depend on an intact cytoskeleton and are regulated by cell adhesion molecules. Tumor necrosis factor alpha (TNF-alpha) is known to induce cell adhesion molecule
Transgene-mediated expression of tumor necrosis factor soluble receptor attenuates morphine tolerance in rats.
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Opiate/narcotic analgesics are the most effective treatments for chronic severe pain, but their clinical utility is often hampered by the development of analgesic tolerance. Recent evidence suggests chronic morphine may activate glial cells to release proinflammatory cytokines. In this study, we
Inhibitory effect of morphine on granulocyte stimulation by tumor necrosis factor and substance P.
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We demonstrate that morphine, at higher concentrations than that effective in the inhibition of spontaneously active cells, can antagonize stimulation of human granulocytes by tumor necrosis factor (TNF) or substance P. The antagonistic effect appears to occur indirectly by way of downregulation of
Modulation of tumor necrosis factor and gamma interferon production by cocaine and morphine in aging mice infected with LP-BM5, a murine retrovirus.
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The actions of retroviral infections, aging, and cocaine and morphine injection on cytokine production were investigated in C57BL/6 female mice. Retroviral infection with LP-BM5 murine leukemia virus was further developed as a model of murine acquired immunodeficiency syndrome (AIDS). The effects of
Synergistic effects of tumour necrosis factor and morphine on gut barrier function.
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OBJECTIVE
To study the effects of tumour necrosis factor (TNF) and morphine on intestinal permeability, intestinal transit and bacterial translocation in the rat.
METHODS
A randomized interventional controlled experiment.
METHODS
University surgery and microbiology research
Intrathecal ultra-low dose naloxone enhances the antihyperalgesic effects of morphine and attenuates tumor necrosis factor-α and tumor necrosis factor-α receptor 1 expression in the dorsal horn of rats with partial sciatic nerve transection.
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BACKGROUND
Glutamate homeostasis and microglia activation play an important role in the development and maintenance of neuropathic pain. We designed this investigation to examine whether ultra-low dose naloxone administered alone or in combination with morphine could alter the concentration of the
Tumor necrosis factor-alpha and its inducer inhibit morphine-induced rewarding effects and sensitization.
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BACKGROUND
Tumor necrosis factor-alpha (TNF-alpha) is emerging as an important modulator of the function of the central nervous system (CNS). We have demonstrated that TNF-alpha or Leu-Ile, a TNF-alpha inducer, inhibits methamphetamine-induced rewarding effects and sensitization. In this study, we
Anti-cancer effects of morphine through inhibition of tumour necrosis factor-alpha release and mRNA expression.
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Morphine is mainly used to relieve pain in the terminal stage of cancer patients. We found that morphine has inhibitory effects on growth of various human cancer cell lines, with IC50 from 2.7 to 8.8 mM, and BALB/3T3 cells, with IC50 of 1.5 mM. Although the IC50 values were relatively high, we
Role of neuroinflammation in morphine tolerance: effect of tumor necrosis factor-α.
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Opioids have been used as potent analgesics in clinics for decades; however, their long-term administration leads to tolerance. Two possible mechanisms for drug tolerance are postulated as within-system and between-systems adaptation. The within-system tolerance is involved in the signal
Effect of morphine on interleukin-1 and tumor necrosis factor alpha production from mouse peritoneal macrophages in vitro.
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OBJECTIVE
To study the influence of morphine on lymphokine production from mouse peritoneal macrophages (PM phi).
METHODS
The productions of interleukin-1 (IL-1) and tumor necrosis factor (TNF-alpha) from PM phi under various concentrations of morphine with or without naloxone were measured by
The mu opioid receptor mediates morphine-induced tumor necrosis factor and interleukin-6 inhibition in toll-like receptor 2-stimulated monocytes.
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BACKGROUND
Morphine possesses immunomodulatory effects but its intrinsic mechanisms, especially in the toll-like receptor 2 (TLR2) signaling pathway, are only partially understood. In this study, we evaluated the effects of morphine on tumor necrosis factor (TNF), interleukin-6 (IL-6), and
Upregulation of tumor necrosis factor-alpha in nucleus accumbens attenuates morphine-induced rewarding in a neuropathic pain model.
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Treatment of neuropathic pain with opioid analgesics remains controversial and a major concern is the risk of addiction. Here, we investigated this issue with spared nerve injury (SNI) model of neuropathic pain in rats and mice. SNI prevented conditioned place preference (CPP) induced by low dose
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