Navegando por Palavras-chave "Neuropathic pain"
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- ItemSomente MetadadadosAntinociceptive effect of the C-terminus of murine S100A9 protein on experimental neuropathic pain(Elsevier B.V., 2008-10-01) Paccola, Carina Cicconi; Gutierrez, Vanessa Pacciari; Longo, Ingrid; Juliano, Luiz [UNIFESP]; Juliano, Maria Aparecida [UNIFESP]; Giorgi, Renata; Butantan Inst; Universidade Federal de São Paulo (UNIFESP)The synthetic peptide identical to the C-terminus of murine S100A9 protein (mS100A9p) has antinociceptive effect on different acute inflammatory pain models. in this study, the effect of mS100A9p was investigated on neuropathic pain induced by chronic constriction injury (CCI) of the sciatic nerve in rats. Hyperalgesia, allodynia, and spontaneous pain were assessed to evaluate nociception. These three signs were detected as early as 2 days after sciatic nerve constriction and lasted for over 14 days after CCI. Rats were treated with different doses of mS100A9p by intraplantar, oral, or intrathecal routes on day 14 after CCI, and nociception was evaluated 1 h later. These three routes of administration blocked hyperalgesia, allodynia and spontaneous pain. the duration of the effect of mS100A9p depends on the route used and phenomenon analyzed. Moreover, intraplantar injection of mS100A9p in the contralateral paw inhibited the hyperalgesia on day 14 days after CCI the results obtained herein demonstrate the antinociceptive effect of the C-terminus of murine S100A9 protein on experimental neuropathic pain, suggesting a potential therapeutic use for it in persistent pain syndromes, assuming that tolerance does not develop to mS100A9p. (C) 2008 Elsevier Inc. All rights reserved.
- ItemSomente MetadadadosRestless Legs Syndrome and Pain Disorders: What's in common?(Springer, 2014-11-01) Goulart, Leonardo Ierardi; Delgado Rodrigues, Raimundo Nonato; Peres, Mario Fernando Prieto [UNIFESP]; Hosp Israelita Albert Einstein; Universidade de Brasília (UnB); Universidade Federal de São Paulo (UNIFESP)Between 10 % and 30 % of the population report chronic pain. More than half of these also have sleep complaints. From considering these data, it can be inferred there is a significant overlapping between these conditions. Restless Legs Syndrome/Willis-Ekbom Disease (RLS/WED) is characterized by complaints of an urge to move frequently associated with dysesthesias. From that perspective, these sensations can also have painful characteristics. By the same token, the presence of comorbid diseases as predicted by a higher prevalence RLS/WED, have many of them with pain as an important complaint. Pain is a multidimensional response involving several levels of expression ranging from somatosensory to emotional. the potential shared mechanisms between RLS/WED and pain may involve sleep deprivation/fragmentation effect, inducing an increase in markers of inflammation and reduction in pain thresholds. These are modulated by several different settings of neurotransmitters with a huge participation of monoaminergic dysfunctional circuits. A thorough comprehension of these mechanisms is of utmost importance for the correct approach and treatment choices.
- ItemSomente MetadadadosThe role of kinin B-1 and B-2 receptors in the persistent pain induced by experimental autoimmune encephalomyelitis (EAE) in mice: Evidence for the involvement of astrocytes(Elsevier B.V., 2013-06-01) Dutra, Rafael C.; Bento, Allisson F.; Leite, Daniela F. P.; Manjavachi, Marianne N.; Marcon, Rodrigo; Bicca, Maira Assuncao; Pesquero, Joao B. [UNIFESP]; Calixto, Joao B.; Universidade Federal de Santa Catarina (UFSC); Universidade Federal de São Paulo (UNIFESP)Multiple sclerosis (MS) is a progressive, demyelinating inflammatory disease of the human central nervous system (CNS). While the primary symptoms of MS affect motor function, it is now recognized that chronic pain is a relevant symptom that affects both animals and MS patients. There is evidence that glial cells, such as astrocytes, play an important role in the development and maintenance of chronic pain. Kinins, notably bradykinin (BK) acting through B-1 (B1R) and B-2 (B2R) receptors, play a central role in pain and inflammatory processes. However, it remains unclear whether kinin receptors are involved in neuropathic pain in MS. Here we investigated by genetic and pharmacological approaches the role of kinin receptors in neuropathic pain behaviors induced in the experimental autoimmune encephalomyelitis (EAE) mouse model. Our results showed that gene deletion or antagonism of kinin receptors, especially B1R, significantly inhibited both tactile and thermal hypersensitivity in EAE animals. By contrast, animals with EAE and treated with a B1R selective agonist displayed a significant increase in tactile hypersensitivity. We also observed a marked increase in B1R mRNA and protein level in the mouse spinal cord 14 days after EAE immunization. Blockade of B1R significantly suppressed the levels of mRNAs for IL-17, IFN-gamma, IL-6, CXCL-1/KC, COX-2 and NOS2, as well as glial activation in the spinal cord. of note, the selective B-1 antagonist DALBK consistently prevented IFN-induced up-regulation of TNF-alpha and IL-6 release in astrocyte culture. Finally, both B1R and B2R antagonists significantly inhibited COX-2 and NOS2 expression in primary astrocyte culture. the B1R was co-localized with immunomarker of astrocytes in the spinal cord of EAE-treated animals. the above data constitute convincing experimental evidence indicating that both kinin receptors, especially the B-1 subtype, exert a critical role in the establishment of persistent hypersensitivity observed in the EAE model, an action that seems to involve a central inflammatory process, possibly acting on astrocytes. Thus, B-1 selective antagonists or drugs that reduce kinin release may have the potential to treat neuropathic pain in patients suffering from MS. (C) 2013 Elsevier Inc. All rights reserved.