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[PMID]:29254302
[Au] Autor:Wang Q; Wang J; Gao D; Li J
[Ad] Endereço:Tumor Center, The First Hospital of Jilin University, Changchun, Jilin, China.
[Ti] Título:Inhibition of PAR2 and TRPA1 signals alleviates neuropathic pain evoked by chemotherapeutic bortezomib.
[So] Source:J Biol Regul Homeost Agents;31(4):977-983, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Bortezomib (BTZ) is generally used as a chemotherapeutic agent for the treatment of multiple myeloma; however, one of the significant limiting complications of BTZ is painful peripheral neuropathy observed during BTZ therapy. There is a lack of drugs which can prevent and/or treat the painful symptoms induced by BTZ, as the underlying molecular mechanism leading to neuropathic pain remains largely unclear. In the present study, we examined engagement of proteinase-activated receptor 2 (PAR2) and transient receptor potential ankyrin 1 (TRPA1) in neuropathic pain induced by BTZ in rats. Our results demonstrated that systemic injection of BTZ increased mechanical pain and cold sensitivity as compared with control animals (P less than 0.05 vs control rats). Our data further showed that blocking respective PAR2 and TRPA1 attenuated mechanical pain and cold sensitivity observed in control rats and BTZ rats (P less than 0.05 vs vehicle control). Notably, the attenuating effect of blocking PAR2 and TRPA1 on mechanical pain and cold sensitivity was significantly less in BTZ rats than that in control rats. In addition, protein expression of PAR2 and TRPA1 was upregulated in the lumbar dorsal root ganglion of BTZ rats, and inhibition of PAR2 decreased the levels of TRPA1 and attenuated its downstream pathways (namely, PKCÉ› and PKA). Overall, we revealed specific signaling pathways leading to neuropathic pain induced by chemotherapeutic BTZ and that blocking PAR2 and TRPA1 in sensory nerves is beneficial to improve neuropathic pain during BTZ intervention.
[Mh] Termos MeSH primário: Analgésicos/farmacologia
Antineoplásicos/efeitos adversos
Bortezomib/efeitos adversos
Neuralgia/prevenção & controle
Oligopeptídeos/farmacologia
Receptor PAR-2/antagonistas & inibidores
Canal de Cátion TRPA1/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Proteínas Quinases Dependentes de AMP Cíclico/genética
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Gânglios Espinais/efeitos dos fármacos
Gânglios Espinais/metabolismo
Gânglios Espinais/fisiopatologia
Regulação da Expressão Gênica
Hiperalgesia/induzido quimicamente
Hiperalgesia/genética
Hiperalgesia/fisiopatologia
Hiperalgesia/prevenção & controle
Masculino
Neuralgia/induzido quimicamente
Neuralgia/genética
Neuralgia/fisiopatologia
Proteína Quinase C-épsilon/genética
Proteína Quinase C-épsilon/metabolismo
Ratos
Ratos Sprague-Dawley
Receptor PAR-2/genética
Receptor PAR-2/metabolismo
Transdução de Sinais
Canal de Cátion TRPA1/genética
Canal de Cátion TRPA1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics); 0 (Antineoplastic Agents); 0 (H-Phe-Ser-Leu-Leu-Arg-Tyr-NH2); 0 (Oligopeptides); 0 (Receptor, PAR-2); 0 (TRPA1 Cation Channel); 0 (Trpa1 protein, rat); 69G8BD63PP (Bortezomib); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 2.7.11.13 (Protein Kinase C-epsilon)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


  2 / 9766 MEDLINE  
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[PMID]:28465077
[Au] Autor:Malet M; Leiguarda C; Gastón G; McCarthy C; Brumovsky P
[Ad] Endereço:Instituto de Investigaciones en Medicina Traslacional (IIMT), Consejo Nacional de Investigaciones Cientiíficas y Técnicas (CONICET) - Austral University, Avenida Juan D. Perón 1500, B1629AHJ, Pilar, Buenos Aires, Argentina.
[Ti] Título:Spinal activation of the NPY Y1 receptor reduces mechanical and cold allodynia in rats with chronic constriction injury.
[So] Source:Peptides;92:38-45, 2017 Jun.
[Is] ISSN:1873-5169
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuropeptide tyrosine (NPY) and its associated receptors Y1R and Y2R have been previously implicated in the spinal modulation of neuropathic pain induced by total or partial sectioning of the sciatic nerve. However, their role in chronic constrictive injuries of the sciatic nerve has not yet been described. In the present study, we analyzed the consequences of pharmacological activation of spinal Y1R, by using the specific Y1R agonist Leu Pro -NPY, in rats with chronic constriction injury (CCI). CCI and sham-injury rats were implanted with a permanent intrathecal catheter (at day 7 after injury), and their response to the administration of different doses (2.5, 5, 7, 10 or 20µg) of Leu Pro -NPY (at a volume of 10µl) through the implanted catheter, recorded 14days after injury. Mechanical allodynia was tested by means of the up-and-down method, using von Frey filaments. Cold allodynia was tested by application of an acetone drop to the affected hindpaw. Intrathecal Leu Pro -NPY induced an increase of mechanical thresholds in rats with CCI, starting at doses of 5µg and becoming stronger with higher doses. Intrathecal Leu Pro also resulted in reductions in the frequency of withdrawal to cold stimuli, although the effect was somewhat more moderate and mostly observed for doses of 7µg and higher. We thus show that spinal activation of the Y1R is able to reduce neuropathic pain due to a chronic constrictive injury and, together with other studies, support the use of a spinal Y1R agonist as a therapeutic agent against chronic pain induced by peripheral neuropathy.
[Mh] Termos MeSH primário: Hiperalgesia/metabolismo
Neuropeptídeo Y/metabolismo
Receptores de Neuropeptídeo Y/metabolismo
Nervo Isquiático/lesões
Neuropatia Ciática/metabolismo
Medula Espinal/metabolismo
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Dor Crônica/metabolismo
Temperatura Baixa
Constrição Patológica/complicações
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Hiperalgesia/etiologia
Injeções Espinhais
Masculino
Neuralgia/metabolismo
Medição da Dor
Limiar da Dor
Ratos
Ratos Sprague-Dawley
Receptores de Neuropeptídeo Y/agonistas
Neuropatia Ciática/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuropeptide Y); 0 (Receptors, Neuropeptide Y)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:27773824
[Au] Autor:Deng L; Lee WH; Xu Z; Makriyannis A; Hohmann AG
[Ad] Endereço:Program in Neuroscience, Department of Psychological and Brain Sciences, Indiana University, Bloomington, IN, USA; Interdisciplinary Biochemistry Graduate Program, Department of Molecular and Cellular Biochemistry, Indiana University, Bloomington, IN, USA.
[Ti] Título:Prophylactic treatment with the tricyclic antidepressant desipramine prevents development of paclitaxel-induced neuropathic pain through activation of endogenous analgesic systems.
[So] Source:Pharmacol Res;114:75-89, 2016 Dec.
[Is] ISSN:1096-1186
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Neuropathic pain impacts approximately 3-4.5% of the global population and remains an unresolved health problem. The management of neuropathic pain has two distinct goals-prevention of development and control of established neuropathic pain. We examined the impact of both prophylactic and therapeutic treatments with the tricyclic antidepressant desipramine on the development and maintenance of toxic neuropathic pain induced by the chemotherapeutic agent paclitaxel. We also investigated the involvement of endogenous analgesic (i.e., endogenous opioid and endocannabinoid) systems in the antinociceptive actions of desipramine in these two distinct phases of neuropathic pain. Chronic subcutaneous infusion of desipramine via osmotic pumps suppressed both the development and maintenance of paclitaxel-induced neuropathic pain. However, only prophylactic desipramine treatment blocked the development of neuropathic pain throughout the three month observation interval; neuropathic pain did not return. The opioid receptor antagonist naloxone blocked the antinociceptive effects of both prophylactic and therapeutic desipramine treatments throughout the entire timecourse of desipramine-induced antinociception. By contrast, cannabinoid CB and CB receptor antagonists partially attenuated the antinociceptive actions of desipramine in a manner that was restricted to the development phase of paclitaxel-induced neuropathic pain only. Paclitaxel decreased cell viability in TMD231 tumor cells in an MTT assay in vitro. Notably, desipramine (1nM-1µM) alone did not alter tumor cell viability and did not prevent the cytotoxic effects of paclitaxel under identical conditions. The highest concentration of desipramine (10µM) reduced tumor cell viability alone and enhanced the cytotoxic effects of paclitaxel. Our study identifies a previously unrecognized preemptive analgesic strategy that prevents development of paclitaxel-induced neuropathic pain, and also dissects receptor mechanisms underlying desipramine-induced antinociceptive effects. This information may be applied to improve current therapeutic strategies with the goal of preventing and managing neuropathic pain induced by chemotherapeutic treatment.
[Mh] Termos MeSH primário: Antidepressivos Tricíclicos/uso terapêutico
Antineoplásicos Fitogênicos/efeitos adversos
Desipramina/uso terapêutico
Neuralgia/induzido quimicamente
Neuralgia/prevenção & controle
Paclitaxel/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Antidepressivos Tricíclicos/farmacologia
Desipramina/farmacologia
Hiperalgesia/induzido quimicamente
Hiperalgesia/prevenção & controle
Masculino
Ratos Sprague-Dawley
Receptores de Canabinoides/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidepressive Agents, Tricyclic); 0 (Antineoplastic Agents, Phytogenic); 0 (Receptors, Cannabinoid); P88XT4IS4D (Paclitaxel); TG537D343B (Desipramine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


  4 / 9766 MEDLINE  
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[PMID]:28969380
[Au] Autor:Vale TA; Symmonds M; Polydefkis M; Byrnes K; Rice ASC; Themistocleous AC; Bennett DLH
[Ad] Endereço:Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
[Ti] Título:Chronic non-freezing cold injury results in neuropathic pain due to a sensory neuropathy.
[So] Source:Brain;140(10):2557-2569, 2017 Oct 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Non-freezing cold injury develops after sustained exposure to cold temperatures, resulting in tissue cooling but not freezing. This can result in persistent sensory disturbance of the hands and feet including numbness, paraesthesia and chronic pain. Both vascular and neurological aetiologies of this pain have been suggested but remain unproven. We prospectively approached patients referred for clinical assessment of chronic pain following non-freezing cold injury between 12 February 2014 and 30 November 2016. Of 47 patients approached, 42 consented to undergo detailed neurological evaluations including: questionnaires to detail pain location and characteristics, structured neurological examination, quantitative sensory testing, nerve conduction studies and skin biopsy for intraepidermal nerve fibre assessment. Of the 42 study participants, all had experienced non-freezing cold injury while serving in the UK armed services and the majority were of African descent (76.2%) and male (95.2%). Many participants reported multiple exposures to cold. The median time between initial injury and referral was 3.72 years. Pain was principally localized to the hands and the feet, neuropathic in nature and in all study participants associated with cold hypersensitivity. Clinical examination and quantitative sensory testing were consistent with a sensory neuropathy. In all cases, large fibre nerve conduction studies were normal. The intraepidermal nerve fibre density was markedly reduced with 90.5% of participants having a count at or below the 0.05 centile of published normative controls. Using the Neuropathic Pain Special Interest Group of the International Association for the Study of Pain grading for neuropathic pain, 100% had probable and 95.2% definite neuropathic pain. Chronic non-freezing cold injury is a disabling neuropathic pain disorder due to a sensory neuropathy. Why some individuals develop an acute painful sensory neuropathy on sustained cold exposure is not yet known, but individuals of African descent appear vulnerable. Screening tools, such as the DN4 questionnaire, and treatment algorithms for neuropathic pain should now be used in the management of these patients.
[Mh] Termos MeSH primário: Lesão por Frio/complicações
Neuralgia/etiologia
Limiar da Dor/fisiologia
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Hiperalgesia/fisiopatologia
Masculino
Condução Nervosa/fisiologia
Neuralgia/psicologia
Exame Neurológico
Medição da Dor
Nervos Periféricos/fisiopatologia
Qualidade de Vida/psicologia
Pele/inervação
Pele/patologia
Inquéritos e Questionários
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx215


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[PMID]:28877966
[Au] Autor:Rosen SF; Ham B; Drouin S; Boachie N; Chabot-Dore AJ; Austin JS; Diatchenko L; Mogil JS
[Ad] Endereço:Department of Psychology and Alan Edwards Centre for Research on Pain, McGill University, Montreal, Quebec H3A 1B1, Canada, and.
[Ti] Título:T-Cell Mediation of Pregnancy Analgesia Affecting Chronic Pain in Mice.
[So] Source:J Neurosci;37(41):9819-9827, 2017 Oct 11.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It has been reported consistently that many female chronic pain sufferers have an attenuation of symptoms during pregnancy. Rats display increased pain tolerance during pregnancy due to an increase in opioid receptors in the spinal cord. Past studies did not consider the role of non-neuronal cells, which are now known to play an important role in chronic pain processing. Using an inflammatory (complete Freund's adjuvant) or neuropathic (spared nerve injury) model of persistent pain, we observed that young adult female mice in early pregnancy switch from a microglia-independent to a microglia-dependent pain hypersensitivity mechanism. During late pregnancy, female mice show no evidence of chronic pain whatsoever. This pregnancy-related analgesia is reversible by intrathecal administration of naloxone, suggesting an opioid-mediated mechanism; pharmacological and genetic data suggest the importance of δ-opioid receptors. We also observe that T-cell-deficient ( and -null mutant) pregnant mice do not exhibit pregnancy analgesia, which can be rescued with the adoptive transfer of CD4 or CD8 T cells from late-pregnant wild-type mice. These results suggest that T cells are a mediator of the opioid analgesia exhibited during pregnancy. Chronic pain symptoms often subside during pregnancy. This pregnancy-related analgesia has been demonstrated for acute pain in rats. Here, we show that pregnancy analgesia can produce a complete cessation of chronic pain behaviors in mice. We show that the phenomenon is dependent on pregnancy hormones (estrogen and progesterone), δ-opioid receptors, and T cells of the adaptive immune system. These findings add to the recent but growing evidence of sex-specific T-cell involvement in chronic pain processing.
[Mh] Termos MeSH primário: Analgesia
Dor Crônica/fisiopatologia
Prenhez/fisiologia
Linfócitos T
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Dor Crônica/induzido quimicamente
Feminino
Hiperalgesia/fisiopatologia
Camundongos
Camundongos Endogâmicos ICR
Camundongos Nus
Microglia/imunologia
Naloxona/farmacologia
Antagonistas de Entorpecentes/farmacologia
Neuralgia/fisiopatologia
Ovariectomia
Gravidez
Receptores Opioides delta/efeitos dos fármacos
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Narcotic Antagonists); 0 (Receptors, Opioid, delta); 36B82AMQ7N (Naloxone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2053-17.2017


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[PMID]:28854251
[Au] Autor:Soon B; Vicenzino B; Schmid AB; Coppieters MW
[Ad] Endereço:Centre of Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, The University of Queensland, Brisbane, Australia.
[Ti] Título:Facilitatory and inhibitory pain mechanisms are altered in patients with carpal tunnel syndrome.
[So] Source:PLoS One;12(8):e0183252, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Preliminary evidence from studies using quantitative sensory testing suggests the presence of central mechanisms in patients with carpal tunnel syndrome (CTS) as apparent by widespread hyperalgesia. Hallmarks of central mechanisms after nerve injuries include nociceptive facilitation and reduced endogenous pain inhibition. Methods to study nociceptive facilitation in CTS so far have been limited to quantitative sensory testing and the integrity of endogenous inhibition remains unexamined. The aim of this study was therefore to investigate changes in facilitatory and inhibitory processing in patients with CTS by studying hypersensitivity following experimentally induced pain (facilitatory mechanisms) and the efficacy of conditioned pain modulation (CPM, inhibitory mechanisms). Twenty-five patients with mild to moderate CTS and 25 age and sex matched control participants without CTS were recruited. Increased pain facilitation was evaluated via injection of hypertonic saline into the upper trapezius. Altered pain inhibition through CPM was investigated through cold water immersion of the foot as the conditioning stimulus and pressure pain threshold over the thenar and hypothenar eminence bilaterally as the test stimulus. The results demonstrated that patients with CTS showed a greater duration (p = 0.047), intensity (p = 0.044) and area (p = 0.012) of pain in response to experimentally induced pain in the upper trapezius and impaired CPM compared to the control participants (p = 0.006). Although typically considered to be driven by peripheral mechanisms, these findings indicate that CTS demonstrates characteristics of altered central processing with increased pain facilitation and reduced endogenous pain inhibition.
[Mh] Termos MeSH primário: Síndrome do Túnel Carpal/fisiopatologia
Dor Crônica/fisiopatologia
Hiperalgesia/fisiopatologia
Dor Nociceptiva/fisiopatologia
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Condicionamento (Psicologia)
Feminino
Mãos/inervação
Mãos/fisiopatologia
Seres Humanos
Injeções Intramusculares
Masculino
Meia-Idade
Músculo Esquelético/inervação
Músculo Esquelético/fisiopatologia
Medição da Dor
Limiar da Dor
Estimulação Física
Pressão
Solução Salina Hipertônica/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Saline Solution, Hypertonic)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170831
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183252


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[PMID]:28827152
[Au] Autor:Kawai S; Yamada T; Matsuura T; Funao T; Nishikawa K
[Ad] Endereço:Department of Anesthesiology, Osaka City University Graduate School of Medicine, Japan.
[Ti] Título:Neuropathic pain attenuates ischemia reperfusion injury through ß2-adrenergic pathway.
[So] Source:Life Sci;187:9-16, 2017 Oct 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: The relationship between neuropathic pain and myocardial infarction (MI) was uncertain because of some medication or underlying diseases. This study investigated the impact of neuropathic pain on ischemia reperfusion injury using isolated rat hearts and cardiomyocytes. MAIN METHODS: Male Sprague-Dawley rats were assigned to the control and allodynia (AL) groups, with the latter subjected to the fifth lumbar spinal-nerve ligation. First, isolated hearts underwent 25-min ischemia and 90-min reperfusion to assess hemodynamic changes and MI area. Second, isolated cardiomyocytes underwent 10-min laser illumination to assess the opening of mitochondrial permeability transition pore (mPTP) and cellular hypercontraction. Lastly, expression of pro-survival kinases was measured in another cardiomyocytes using flow cytometry. AL-treated hearts were concomitantly examined regarding the involvement of ß-adrenergic pathways by esmolol (ESM), ß1-blocker (100µM, AL+ESM), and ICI118551 (ICI), ß2-blocker (50nM, AL+ICI). KEY FINDINGS: All hemodynamic variables did not change significantly in between-group comparisons except at 30min of reperfusion. MI area decreased remarkably in the AL and AL+ESM groups after 90-min reperfusion. The AL+ICI group significantly increased it as compared with the AL and AL+ESM groups. Similarly, the AL and AL+ESM groups significantly inhibited mPTP opening and cellular hypercontraction, whereas the AL+ICI group reversed these effects. Enhanced expression of pro-survival kinases was observed in the AL and AL+ESM groups, but the AL+ICI group abolished this enhancement. SIGNIFICANCE: Our findings suggested that neuropathic pain possessed cardioprotective effects through inhibiting mPTP opening. The underlying mechanisms were possibly regulated by ß2-adrenergic activation and pro-survival kinase expression in cardiomyocytes.
[Mh] Termos MeSH primário: Proteínas de Transporte da Membrana Mitocondrial/efeitos dos fármacos
Infarto do Miocárdio/patologia
Neuralgia/metabolismo
Propanolaminas/farmacologia
Traumatismo por Reperfusão/prevenção & controle
[Mh] Termos MeSH secundário: Antagonistas de Receptores Adrenérgicos beta 1/farmacologia
Antagonistas de Receptores Adrenérgicos beta 2/farmacologia
Animais
Hemodinâmica/efeitos dos fármacos
Hemodinâmica/fisiologia
Hiperalgesia/patologia
Hiperalgesia/prevenção & controle
Preparação de Coração Isolado
Ligadura
Masculino
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Infarto do Miocárdio/fisiopatologia
Miócitos Cardíacos/metabolismo
Neuralgia/complicações
Fosfotransferases/efeitos dos fármacos
Fosfotransferases/metabolismo
Fatores de Proteção
Ratos
Medula Espinal
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-1 Receptor Antagonists); 0 (Adrenergic beta-2 Receptor Antagonists); 0 (Mitochondrial Membrane Transport Proteins); 0 (Propanolamines); 0 (mitochondrial permeability transition pore); 46OL1UC10R (ICI 118551); EC 2.7.- (Phosphotransferases); MDY902UXSR (esmolol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE


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[PMID]:28806224
[Au] Autor:Hsieh MC; Ho YC; Lai CY; Wang HH; Lee AS; Cheng JK; Chau YP; Peng HY
[Ad] Endereço:From the Department of Physiology, College of Medicine, National Taiwan University, Taipei, Taiwan (M.-C.H.); Department of Medicine, Mackay Medical College, New Taipei, Taiwan (M.-C.H., Y.-C.H., C.-Y.L., H.-H.W., A.-S.L., J.-K.C., Y.-P.C., H.-Y.P.); Department of Veterinary Medicine, College of Veterinary Medicine, National Chung-Hsing University, Taichung, Taiwan (C.-Y.L.); and Department of Anesthesiology, Mackay Memorial Hospital, Taipei, Taiwan (J.-K.C.).
[Ti] Título:Bromodomain-containing Protein 4 Activates Voltage-gated Sodium Channel 1.7 Transcription in Dorsal Root Ganglia Neurons to Mediate Thermal Hyperalgesia in Rats.
[So] Source:Anesthesiology;127(5):862-877, 2017 Nov.
[Is] ISSN:1528-1175
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Bromodomain-containing protein 4 binds acetylated promoter histones and promotes transcription; however, the role of bromodomain-containing protein 4 in inflammatory hyperalgesia remains unclear. METHODS: Male Sprague-Dawley rats received hind paw injections of complete Freund's adjuvant to induce hyperalgesia. The dorsal root ganglia were examined to detect changes in bromodomain-containing protein 4 expression and the activation of genes involved in the expression of voltage-gated sodium channel 1.7, which is a key pain-related ion channel. RESULTS: The intraplantar complete Freund's adjuvant injections resulted in thermal hyperalgesia (4.0 ± 1.5 s; n = 7). The immunohistochemistry and immunoblotting results demonstrated an increase in the bromodomain-containing protein 4-expressing dorsal root ganglia neurons (3.78 ± 0.38 fold; n = 7) and bromodomain-containing protein 4 protein levels (2.62 ± 0.39 fold; n = 6). After the complete Freund's adjuvant injection, histone H3 protein acetylation was enhanced in the voltage-gated sodium channel 1.7 promoter, and cyclin-dependent kinase 9 and phosphorylation of RNA polymerase II were recruited to this area. Furthermore, the voltage-gated sodium channel 1.7-mediated currents were enhanced in neurons of the complete Freund's adjuvant rats (55 ± 11 vs. 19 ± 9 pA/pF; n = 4 to 6 neurons). Using bromodomain-containing protein 4-targeted antisense small interfering RNA to the complete Freund's adjuvant-treated rats, the authors demonstrated a reduction in the expression of bromodomain-containing protein 4 (0.68 ± 0.16 fold; n = 7), a reduction in thermal hyperalgesia (7.5 ± 1.5 s; n = 7), and a reduction in the increased voltage-gated sodium channel 1.7 currents (21 ± 4 pA/pF; n = 4 to 6 neurons). CONCLUSIONS: Complete Freund's adjuvant triggers enhanced bromodomain-containing protein 4 expression, ultimately leading to the enhanced excitability of nociceptive neurons and thermal hyperalgesia. This effect is likely mediated by the enhanced expression of voltage-gated sodium channel 1.7.
[Mh] Termos MeSH primário: Gânglios Espinais/metabolismo
Hiperalgesia/metabolismo
Canal de Sódio Disparado por Voltagem NAV1.7/metabolismo
Neurônios/metabolismo
Proteínas Nucleares/metabolismo
Fatores de Transcrição/metabolismo
Transcrição Genética/fisiologia
[Mh] Termos MeSH secundário: Animais
Gânglios Espinais/patologia
Temperatura Alta/efeitos adversos
Hiperalgesia/genética
Hiperalgesia/patologia
Masculino
Canal de Sódio Disparado por Voltagem NAV1.7/genética
Neurônios/patologia
Proteínas Nucleares/genética
Ratos
Ratos Sprague-Dawley
Fatores de Transcrição/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Brd4 protein, mouse); 0 (NAV1.7 Voltage-Gated Sodium Channel); 0 (Nuclear Proteins); 0 (Scn9a protein, rat); 0 (Transcription Factors)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE
[do] DOI:10.1097/ALN.0000000000001809


  9 / 9766 MEDLINE  
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[PMID]:28783046
[Au] Autor:Martin LJ; Smith SB; Khoutorsky A; Magnussen CA; Samoshkin A; Sorge RE; Cho C; Yosefpour N; Sivaselvachandran S; Tohyama S; Cole T; Khuong TM; Mir E; Gibson DG; Wieskopf JS; Sotocinal SG; Austin JS; Meloto CB; Gitt JH; Gkogkas C; Sonenberg N; Greenspan JD; Fillingim RB; Ohrbach R; Slade GD; Knott C; Dubner R; Nackley AG; Ribeiro-da-Silva A; Neely GG; Maixner W; Zaykin DV; Mogil JS; Diatchenko L
[Ad] Endereço:Department of Psychology and Alan Edwards Centre for Research on Pain, McGill University, Montreal, Quebec, Canada.
[Ti] Título:Epiregulin and EGFR interactions are involved in pain processing.
[So] Source:J Clin Invest;127(9):3353-3366, 2017 Sep 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The EGFR belongs to the well-studied ErbB family of receptor tyrosine kinases. EGFR is activated by numerous endogenous ligands that promote cellular growth, proliferation, and tissue regeneration. In the present study, we have demonstrated a role for EGFR and its natural ligand, epiregulin (EREG), in pain processing. We show that inhibition of EGFR with clinically available compounds strongly reduced nocifensive behavior in mouse models of inflammatory and chronic pain. EREG-mediated activation of EGFR enhanced nociception through a mechanism involving the PI3K/AKT/mTOR pathway and matrix metalloproteinase-9. Moreover, EREG application potentiated capsaicin-induced calcium influx in a subset of sensory neurons. Both the EGFR and EREG genes displayed a genetic association with the development of chronic pain in several clinical cohorts of temporomandibular disorder. Thus, EGFR and EREG may be suitable therapeutic targets for persistent pain conditions.
[Mh] Termos MeSH primário: Dor Crônica/metabolismo
Epirregulina/genética
Epirregulina/fisiologia
Receptor do Fator de Crescimento Epidérmico/fisiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Animais
Comportamento Animal
Estudos de Casos e Controles
Estudos de Coortes
Drosophila melanogaster
Feminino
Seres Humanos
Hiperalgesia/metabolismo
Inflamação
Ligantes
Masculino
Metaloproteinase 9 da Matriz/metabolismo
Camundongos
Mutação
Neurônios/metabolismo
Manejo da Dor
Fosforilação
Polimorfismo de Nucleotídeo Único
Ligação Proteica
Transdução de Sinais
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epiregulin); 0 (Ereg protein, mouse); 0 (Ligands); EC 2.7.10.1 (EGFR protein, mouse); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE


  10 / 9766 MEDLINE  
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[PMID]:28777065
[Au] Autor:Renno WM; Benov L; Khan KM
[Ad] Endereço:Departments of 1 Anatomy and.
[Ti] Título:Possible role of antioxidative capacity of (-)-epigallocatechin-3-gallate treatment in morphological and neurobehavioral recovery after sciatic nerve crush injury.
[So] Source:J Neurosurg Spine;27(5):593-613, 2017 Nov.
[Is] ISSN:1547-5646
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE This study examined the capacity of the major polyphenolic green tea extract (-)-epigallocatechin-3-gallate (EGCG) to suppress oxidative stress and stimulate the recovery and prompt the regeneration of sciatic nerve after crush injury. METHODS Adult male Wistar rats were randomly assigned to one of 4 groups: 1) Naïve, 2) Sham (sham injury, surgical control group), 3) Crush (sciatic nerve crush injury treated with saline), and 4) Crush+EGCG (sciatic nerve crush injury treated with intraperitoneally administered EGCG, 50 mg/kg). All animals were tested for motor and sensory neurobehavioral parameters throughout the study. Sciatic nerve and spinal cord tissues were harvested and processed for morphometric and stereological analysis. For the biochemical assays, the time points were Day 1, Day 7, Day 14, and Day 28 after nerve injury. RESULTS After sciatic nerve crush injury, the EGCG-treated animals (Crush+EGCG group) showed significantly better recovery of foot position and toe spread and 50% greater improvement in motor recovery than the saline-treated animals (Crush group). The Crush+EGCG group displayed an early hopping response at the beginning of the 3rd week postinjury. Animals in the Crush+EGCG group also showed a significant reduction in mechanical allodynia and hyperalgesia latencies and significant improvement in recovery from nociception deficits in both heat withdrawal and tail flick withdrawal latencies compared with the Crush group. In both the Crush+EGCG and Crush groups, quantitative evaluation revealed significant morphological evidence of neuroregeneration according to the following parameters: mean cross-sectional area of axons, myelin thickness in the sciatic nerve (from Week 4 to Week 8), increase of myelin basic protein concentration and gene expression in both the injured sciatic nerve and spinal cord, and fiber diameter to axon diameter ratio and myelin thickness to axon diameter ratio at Week 2 after sciatic nerve injury. However, the axon area remained much smaller in both the Crush+EGCG and Crush groups compared with the Sham and Naïve groups. The number of axons per unit area was significantly decreased in the Crush+EGCG and Crush groups compared with controls. Sciatic nerve injury produced generalized oxidative stress manifested as a significant increase of isoprostanes in the urine and decrease of the total antioxidant capacity (TAC) of the blood from Day 7 until Day 14. EGCG-treated rats showed significantly less increase of isoprostanes than saline-treated animals and also showed full recovery of TAC levels by Day 14 after nerve injury. In spinal cord tissue analysis, EGCG-treated animals showed induced glutathione reductase and suppressed induction of heme oxygenase 1 gene expression compared with nontreated animals. CONCLUSIONS EGCG treatment suppressed the crush-induced production of isoprostanes and stimulated the recovery of the TAC and was associated with remarkable alleviation of motor and sensory impairment and significant histomorphological evidence of neuronal regeneration following sciatic nerve crush injury in rats. The findings of this study suggest that EGCG can be used as an adjunctive therapeutic remedy for nerve injury. However, further investigations are needed to establish the antioxidative mechanism involved in the regenerative process after nerve injury. Only upregulation of glutathione reductase supports the idea that EGCG is acting indirectly via induction of enzymes or transcription factors.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Catequina/análogos & derivados
Lesões por Esmagamento/tratamento farmacológico
Traumatismos dos Nervos Periféricos/tratamento farmacológico
Nervo Isquiático/efeitos dos fármacos
Nervo Isquiático/lesões
[Mh] Termos MeSH secundário: Animais
Axônios/efeitos dos fármacos
Axônios/patologia
Catequina/farmacologia
Lesões por Esmagamento/patologia
Lesões por Esmagamento/fisiopatologia
Modelos Animais de Doenças
Hiperalgesia/tratamento farmacológico
Hiperalgesia/patologia
Hiperalgesia/fisiopatologia
Masculino
Atividade Motora/efeitos dos fármacos
Atividade Motora/fisiologia
Regeneração Nervosa/efeitos dos fármacos
Regeneração Nervosa/fisiologia
Fármacos Neuroprotetores/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Estresse Oxidativo/fisiologia
Traumatismos dos Nervos Periféricos/patologia
Traumatismos dos Nervos Periféricos/fisiopatologia
RNA Mensageiro/metabolismo
Distribuição Aleatória
Ratos Wistar
Recuperação de Função Fisiológica/efeitos dos fármacos
Nervo Isquiático/patologia
Nervo Isquiático/fisiopatologia
Neuropatia Ciática/tratamento farmacológico
Neuropatia Ciática/patologia
Neuropatia Ciática/fisiopatologia
Medula Espinal/efeitos dos fármacos
Medula Espinal/patologia
Medula Espinal/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Neuroprotective Agents); 0 (RNA, Messenger); 8R1V1STN48 (Catechin); BQM438CTEL (epigallocatechin gallate)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170805
[St] Status:MEDLINE
[do] DOI:10.3171/2016.10.SPINE16218



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