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[PMID]:29381725
[Au] Autor:Henssen DJHA; Kurt E; van Cappellen van Walsum AM; Arnts I; Doorduin J; Kozicz T; van Dongen R; Bartels RHMA
[Ad] Endereço:Department of Anatomy, Donders Institute for Brain, Cognition & Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands.
[Ti] Título:Long-term effect of motor cortex stimulation in patients suffering from chronic neuropathic pain: An observational study.
[So] Source:PLoS One;13(1):e0191774, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Motor cortex stimulation (MCS) was introduced as a last-resort treatment for chronic neuropathic pain. Over the years, MCS has been used for the treatment of various pain syndromes but long-term follow-up is unknown. METHODS: This paper reports the results of MCS from 2005 until 2012 with a 3-year follow-up. Patients who suffered from chronic neuropathic pain treated with MCS were studied. The analgesic effect was determined as successful by decrease in pain-intensity on the visual analog scale (VAS) of at least 40%. The modifications in drug regimens were monitored with use of the medication quantification scale (MQS). Stimulation parameters and complications were also noted. Interference of pain with quality of life (QoL), the Quality of Life Index (QLI), was determined with use of a specific subset of questions from the MPQ-DLV score. RESULTS: Eighteen patients were included. Mean pre-operative VAS changed from 89.4 ± 11.2 to 53.1 ± 25.0 after three years of follow-up (P < 0.0001). A successful outcome was achieved in seven responders (38.9%). All patients in the responder group suffered from pain caused by a central lesion. With regard to all the patients with central pain lesions (n = 10) and peripheral lesions (n = 8), a significant difference in response to MCS was noticed (P = 0.002). MQS scores and QLI-scores diminished during the follow-up period (P = 0.210 and P = 0.007, respectively). CONCLUSION: MCS seems a promising therapeutic option for patients with refractory pain syndromes of central origin.
[Mh] Termos MeSH primário: Dor Crônica/fisiopatologia
Estimulação Encefálica Profunda/métodos
Córtex Motor/fisiopatologia
Neuralgia/fisiopatologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Analgésicos/administração & dosagem
Analgésicos/uso terapêutico
Dor Crônica/diagnóstico por imagem
Dor Crônica/tratamento farmacológico
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Córtex Motor/diagnóstico por imagem
Neuralgia/diagnóstico por imagem
Neuralgia/tratamento farmacológico
Medição da Dor
Qualidade de Vida
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Analgesics)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191774


  2 / 10220 MEDLINE  
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[PMID]:29441918
[Au] Autor:Wang S; Li A; Guo S
[Ti] Título:Ligustrazine attenuates neuropathic pain by inhibition of JAK/STAT3 pathway in a rat model of chronic constriction injury.
[So] Source:Pharmazie;71(7):408-412, 2016 Jul 07.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:AIM: Neuropathic pain is a common clinical complication of nerve injury, and the effective treatment of neuropathic pain is still challenging. Ligustrazine is mainly used for the treatment of cardiovascular disease and its role in neuropathic pain is less investigated. The purpose of our study was to explore the effects of ligustrazine on neuropathic pain, as well as the underlying molecular mechanism. METHODS: Neuropathic pain was induced by chronic constriction injury (CCI) of the right sciatic nerve in Sprague-Dawley (SD) rats. After CCI, rats received ligustrazine, IL-6, or both. Mechanical withdrawal threshold (MWT) and paw withdrawal thermal latency (PWTL) were assessed on days 1, 3, 7, and 14 after surgery. Expression levels of tumor necrosis factor (TNF)-α, interleukin (IL)-ß, IL-2, and phosphorylation of Signal Transducer and Activator of Transcription (STAT) 3 were analyzed. RESULTS: Our results showed that both MWT and PWTL were significantly decreased by CCI on days 1, 3, 7 and 14 compared to sham group, however, ligustrazine reversed this effects. Additionally, the elevated levels of TNF-α, IL-1ß, and IL-2 in CCI spinal cord were inhibited by ligustrazine. Quantitative real-time (qRT-PCR) and Western blotting analysis showed that the test substance reduced the elevated expression of pSTAT3 in the spinal cord induced by CCI, and while IL-6 administration reversed the levels as well as the behavior responses. CONCLUSION: Our results suggest that ligustrazine could effectively attenuate neuropathic pain by inhibition of Janus Kinase (JAK)/STAT3 pathway in CCI rats.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/uso terapêutico
Constrição Patológica/complicações
Neuralgia/tratamento farmacológico
Pirazinas/uso terapêutico
Fator de Transcrição STAT3/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Comportamento Animal/efeitos dos fármacos
Citocinas/antagonistas & inibidores
Citocinas/biossíntese
Temperatura Alta
Masculino
Neuralgia/etiologia
Neuralgia/psicologia
Limiar da Dor/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Fator de Transcrição STAT3/biossíntese
Nervo Isquiático/lesões
Medula Espinal/efeitos dos fármacos
Medula Espinal/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cytokines); 0 (Pyrazines); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, rat); V80F4IA5XG (tetramethylpyrazine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6546


  3 / 10220 MEDLINE  
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[PMID]:29409869
[Au] Autor:Tateiwa H; Kawano T; Nishigaki A; Yamanaka D; Aoyama B; Shigematsu-Locatelli M; Eguchi S; Locatelli FM; Yokoyama M
[Ad] Endereço:Department of Anesthesiology and Intensive Care Medicine, Kochi Medical School, Nankoku, Kochi, Japan.
[Ti] Título:The role of hippocampal brain-derived neurotrophic factor in age-related differences in neuropathic pain behavior in rats.
[So] Source:Life Sci;197:56-66, 2018 Mar 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: This study was aimed to explore the contribution of central brain-derived neurotrophic factor (BDNF) in the neuropathic pain pathogenesis using an aged rodent model. MAIN METHODS: Adult and aged rats were randomly assigned to either a sciatic nerve ligation (SNL) group or a control skin sham surgery group. Sensory behavioral testing were performed on the day before surgery and on the 3rd, 7th, 14th, and 21st days after surgery, followed by measurement of BDNF protein levels in different brain regions. In another experiment, the hippocampal BDNF gene expression after SNL surgery was assessed at different time-points. Furthermore, the analgesic effects of intranasal BDNF administration were tested in SNL animals. KEY FINDINGS: Our behavioral results demonstrated that the hyperalgesia-like behavior after painful nerve injury has a higher incidence in aged rats compared with in adult animals. In particular, the hippocampal BDNF levels were inversely correlated with the probability of hyperalgesia-type behavior, in both brain-region specific and age-dependent manner. Time-course analysis showed that the hippocampal levels of BDNF mRNA in aged and adult rats started to decrease 7 and 14 days after surgery, respectively. However, the decrease was more pronounced in aged animals. Moreover, the repeated intranasal BDNF treatment could restore the central BDNF signaling, counteracting the age-related exacerbation of hyperalgesic behavior. SIGNIFICANCE: Our findings imply that hippocampal BDNF may be related with the pathogenesis of elderly neuropathic pain. Pharmacological data further suggest that brain BDNF may be modifiable in aged neuropathic animals, and therefore, represent a promising target for intervention.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Comportamento Animal
Fator Neurotrófico Derivado do Encéfalo/biossíntese
Regulação da Expressão Gênica
Hipocampo/metabolismo
Neuralgia/metabolismo
[Mh] Termos MeSH secundário: Envelhecimento/patologia
Animais
Hipocampo/patologia
Masculino
Neuralgia/patologia
RNA Mensageiro/biossíntese
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (RNA, Messenger)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180208
[St] Status:MEDLINE


  4 / 10220 MEDLINE  
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[PMID]:27770598
[Au] Autor:Isomura T; Sumitani M; Matsudaira K; Kawaguchi M; Inoue R; Hozumi J; Tanaka T; Oshima H; Mori K; Taketomi S; Inui H; Tahara K; Yamagami R; Hayakawa K
[Ad] Endereço:Clinical Study Support Inc., Nagoya, Japan.
[Ti] Título:Development of the Japanese Version of the Leeds Assessment of the Neuropathic Symptoms and Signs Pain Scale: Diagnostic Utility in a Clinical Setting.
[So] Source:Pain Pract;17(6):800-807, 2017 Jul.
[Is] ISSN:1533-2500
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: We aimed to assess the diagnostic utility of the linguistically validated Japanese version of the Leeds Assessment of Neuropathic Symptoms and Signs Pain Scale (LANSS-J) as a screening tool for neuropathic pain in the clinical setting. METHODS: Patients with neuropathic pain or nociceptive pain who were 20 to 85 years of age were included. Sensitivity and specificity using the original cutoff value of 12 were assessed to evaluate the diagnostic utility of the LANSS-J. Sensitivity and specificity with possible cutoff values were calculated, along with area under the receiver operating characteristic curve. We then evaluated agreement regarding assessment of the LANSS-J by two investigators. We used the intraclass correlation coefficient (ICC) for the total score and Cohen's kappa coefficient for each item. RESULTS: Data for patients with neuropathic pain (n = 30) and those with nociceptive pain (n = 29) were analyzed. With a cutoff of 12, the sensitivity was 63.3% (19/30) and the specificity 93.1% (27/29). Sensitivity improved substantially with a cutoff of ≤ 11 (≥ 83.3%, 25/30). High specificity (93.1%, 27/29) was sustained with a cutoff of 9 to 12. The ICC for the total score was 0.85, indicating sufficient agreement. Kappa coefficients ranged from 0.68 to 0.84. CONCLUSIONS: The LANSS-J is a valid screening tool for detecting neuropathic pain. Our results suggest that employing the original cutoff value provides high specificity, although a lower cutoff value of 10 or 11 (with its high specificity maintained) may be more beneficial when pain attributed to neuropathic mechanisms is suspected in Japanese patients.
[Mh] Termos MeSH primário: Neuralgia/diagnóstico
Neuralgia/epidemiologia
Medição da Dor/métodos
Medição da Dor/normas
Tradução
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Feminino
Seres Humanos
Japão/epidemiologia
Masculino
Meia-Idade
Medição da Dor/tendências
Reprodutibilidade dos Testes
Inquéritos e Questionários
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1111/papr.12528


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[PMID]:28451639
[Au] Autor:Kanda H; Kobayashi K; Yamanaka H; Okubo M; Noguchi K
[Ad] Endereço:Department of Anatomy and Neuroscience, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan.
[Ti] Título:Microglial TNFα Induces COX2 and PGI2 Synthase Expression in Spinal Endothelial Cells during Neuropathic Pain.
[So] Source:eNeuro;4(2), 2017 Mar-Apr.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prostaglandins (PGs) are typical lipid mediators that play a role in homeostasis and disease. They are synthesized from arachidonic acid by cyclooxygenase 1 (COX1) and COX2. Although COX2 has been reported to be upregulated in the spinal cord after nerve injury, its expression and functional roles in neuropathic pain remain unclear. In this study, we investigated the expression of Cox2, PGI2 synthase (Pgis), and prostaglandin I2 receptor (IP receptor) mRNA in the rat spinal cord after spared nerve injury (SNI). Levels of Cox2 and Pgis mRNA increased in endothelial cells from 24 to 48 h after nerve injury. IP receptor mRNA was constitutively expressed in dorsal horn neurons. A COX2 inhibitor and IP receptor antagonists attenuated pain behavior in the early phase of neuropathic pain. Furthermore, we examined the relationship between COX2 and tumor necrosis factor-α (TNFα) in the spinal cord of a rat SNI model. Levels of TNFα mRNA transiently increased in the spinal microglia 24 h after SNI. The TNF receptors Tnfr1 and Tnfr2 mRNA were colocalized with COX2. Intrathecal injection of TNFα induced Cox2 and Pgis mRNA expression in endothelial cells. These results revealed that microglia-derived TNFα induced COX2 and PGIS expression in spinal endothelial cells and that endothelial PGI2 played a critical role in neuropathic pain via neuronal IP receptor. These findings further suggest that the glia-endothelial cell interaction of the neurovascular unit via transient TNFα is involved in the generation of neuropathic pain.
[Mh] Termos MeSH primário: Ciclo-Oxigenase 2/metabolismo
Sistema Enzimático do Citocromo P-450/metabolismo
Células Endoteliais/enzimologia
Oxirredutases Intramoleculares/metabolismo
Microglia/metabolismo
Neuralgia/metabolismo
Medula Espinal/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Inflamação/enzimologia
Masculino
Traumatismos dos Nervos Periféricos/metabolismo
RNA Mensageiro
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Tumor Necrosis Factor-alpha); 9035-51-2 (Cytochrome P-450 Enzyme System); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (Ptgs2 protein, rat); EC 5.3.- (Intramolecular Oxidoreductases); EC 5.3.99.4 (prostacyclin synthetase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


  6 / 10220 MEDLINE  
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[PMID]:29279555
[Au] Autor:Masuda R; Ajimi J; Murata T
[Ad] Endereço:Department of Anesthesiology, Tokai University Hachioji Hospital.
[Ti] Título:Pharmacotherapy for Neuropathic Pain in Japan.
[So] Source:J Nippon Med Sch;84(6):258-267, 2017.
[Is] ISSN:1347-3409
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Neuropathic pain (NeP) results from injury to, or disease of, the peripheral or central components of the neural systems involved in pain. In contrast to inflammatory pain, NeP can persist after healing from the initial injury has resolved. Antipyretic agents, such as non-steroidal anti-inflammatory drugs, steroids, and acetaminophen are ineffective, while specific agents such as gabapentinoids, antidepressants, antiepileptics, and opioids are effective in treating NeP. In this review, we address the definition of NeP, pharmacotherapy for NeP in Japan, pain classification, setting goals for successful NeP medication, and the Japanese algorithm for the pharmacotherapy of NeP with specific prescription guidance.
[Mh] Termos MeSH primário: Aminas/administração & dosagem
Analgésicos Opioides/administração & dosagem
Anticonvulsivantes/administração & dosagem
Antidepressivos/administração & dosagem
Ácidos Cicloexanocarboxílicos/administração & dosagem
Cloridrato de Duloxetina/administração & dosagem
Neuralgia/tratamento farmacológico
Pregabalina/administração & dosagem
Ácido gama-Aminobutírico/administração & dosagem
[Mh] Termos MeSH secundário: Idoso
Algoritmos
Aminas/efeitos adversos
Analgésicos Opioides/efeitos adversos
Anticonvulsivantes/efeitos adversos
Antidepressivos/efeitos adversos
Ácidos Cicloexanocarboxílicos/efeitos adversos
Esquema de Medicação
Cloridrato de Duloxetina/efeitos adversos
Feminino
Seres Humanos
Japão
Neuralgia/classificação
Manejo da Dor
Pregabalina/efeitos adversos
Ácido gama-Aminobutírico/efeitos adversos
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Amines); 0 (Analgesics, Opioid); 0 (Anticonvulsants); 0 (Antidepressive Agents); 0 (Cyclohexanecarboxylic Acids); 55JG375S6M (Pregabalin); 56-12-2 (gamma-Aminobutyric Acid); 6CW7F3G59X (gabapentin); 9044SC542W (Duloxetine Hydrochloride)
[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:171228
[St] Status:MEDLINE
[do] DOI:10.1272/jnms.84.258


  7 / 10220 MEDLINE  
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[PMID]:29277615
[Au] Autor:Li J; Sun Y; Ding G; Jiang F
[Ad] Endereço:Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.
[Ti] Título:Persistent pain accelerates xenograft tumor growth of breast cancer in rat.
[So] Source:Biochem Biophys Res Commun;495(4):2432-2438, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pain occurs at all stages of the patients who suffer from cancer. Owing to surgery and bone metastasis, breast cancer patients were usually disturbed by persistent pain. However, the pain-relief-right has not been respected enough in clinical cancer treatment. Whether pain has any adverse effects on cancer development is still unclear. In order to uncover this question, we established two preclinical animal models to explore the effects of pain on the tumor. For the first model, we mimicked neuropathic pain by sciatic nerve ligation on rats with xenograft tumor subcutaneously. For the second model, we mimicked the bone cancer pain by injecting tumor cell suspension into the tibial medullary cavity of rats with xenograft tumor subcutaneously. The rats with persistent pain showed higher tumor volume and tumor weight compared with the group without pain. Interestingly, when the neuropathic pain and bone cancer pain were relieved by drug administration, both the tumor volume and tumor weight were lowered compared with the group without pain relief. In summary, our study indicated that persistent pain acted as a contributing factor to tumor growth. Moreover, the pain relief could weakened the accelerating role of pain in tumor growth. Thus, we should be paid more attention to the cancer patients with persistent pain as well as cancer treatment.
[Mh] Termos MeSH primário: Neoplasias da Mama/fisiopatologia
Dor do Câncer/fisiopatologia
Dor Crônica/fisiopatologia
Neuralgia/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/complicações
Dor do Câncer/complicações
Dor do Câncer/etiologia
Linhagem Celular Tumoral
Proliferação Celular
Dor Crônica/etiologia
Feminino
Invasividade Neoplásica
Neuralgia/etiologia
Medição da Dor
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[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:171227
[St] Status:MEDLINE


  8 / 10220 MEDLINE  
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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


  9 / 10220 MEDLINE  
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[PMID]:29217355
[Au] Autor:Wang X; Zhang G; Qiao Y; Feng C; Zhao X
[Ad] Endereço:Department of Anesthesiology, The Second Hospital of Shandong University, 247 Bei Yuan Street, Jinan 250033, China.
[Ti] Título:Crocetin attenuates spared nerve injury-induced neuropathic pain in mice.
[So] Source:J Pharmacol Sci;135(4):141-147, 2017 Dec.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Crocetin is the main component of saffron and exhibits anti-oxidative and anti-inflammatory effects. Neuroinflammation and oxidative stress have been recognized to play a crucial role in the pathogenesis of neuropathic pain. We investigated the effect of crocetin in a mouse model with neuropathic pain induced by spared nerve injury (SNI). Crocetin was intrathecally perfused at various doses for up to 12 days starting 3 days before the surgery. Behavioral tests were performed to determine pain sensitivity. The concentrations of proinflammatory cytokines tumor necrosis factor (TNF-α) and interleukin-1ß (IL-1ß) were measured to assess neuroinflammation. In addition, the enzymatic activity of superoxide dismutase (SOD) was measured to reveal the oxidative stress level. We found that repeated treatment with crocetin dose-dependently attenuated mechanical and thermal allodynia in SNI mice. In addition, treatment with high dose of crocetin reduced SNI-induced increase of TNF-α and IL-1ß. Crocetin also restored the activity of mitochondrial MnSOD which was reduced in the sciatic nerve and the spinal cord of SNI mice. Collectively, our data demonstrate that crocetin effectively attenuates the neuropathic pain and significantly suppresses oxidative stress and neuroinflammation in the SNI mouse model, supporting the potential of crocetin in the treatment against neuropathic pain.
[Mh] Termos MeSH primário: Carotenoides/administração & dosagem
Carotenoides/farmacologia
Neuralgia/tratamento farmacológico
Neuralgia/etiologia
Traumatismos dos Nervos Periféricos/complicações
Fitoterapia
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios
Antioxidantes
Biomarcadores
Carotenoides/isolamento & purificação
Crocus/química
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Mediadores da Inflamação/metabolismo
Interleucina-1beta/metabolismo
Masculino
Camundongos Endogâmicos
Neuralgia/diagnóstico
Neuralgia/metabolismo
Estresse Oxidativo
Nervo Isquiático/metabolismo
Medula Espinal
Superóxido Dismutase
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antioxidants); 0 (Biomarkers); 0 (Inflammation Mediators); 0 (Interleukin-1beta); 0 (Tumor Necrosis Factor-alpha); 20TC155L9C (crocetin); 36-88-4 (Carotenoids); EC 1.15.1.1 (Superoxide Dismutase)
[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:171209
[St] Status:MEDLINE


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[PMID]:29177353
[Au] Autor:Shah R; Zhou A; Wagner CR
[Ad] Endereço:Department of Medicinal Chemistry University of Minnesota, USA. wagne003@umn.edu.
[Ti] Título:Switch-on fluorescent/FRET probes to study human histidine triad nucleotide binding protein 1 (hHint1), a novel target for opioid tolerance and neuropathic pain.
[So] Source:Org Biomol Chem;15(48):10230-10237, 2017 Dec 13.
[Is] ISSN:1477-0539
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Histidine Triad Nucleotide Binding Protein 1 (Hint1) has emerged to be an important post-synaptic protein associated with a variety of central nervous system disorders such as pain, addiction, and schizophrenia. Recently, inhibition of histidine nucleotide binding protein 1 (Hint1) with a small nucleoside inhibitor has shown promise as a new therapeutic strategy for the treatment of neuropathic pain. Herein, we describe the first rationally designed small molecule switch-on probes with dual fluorescence and FRET properties to study Hint1. Two non-natural fluorescent nucleosides with a fluorescent lifetime of 20 and 25 ns were each coupled through a linker to the indole ring, i.e. probes 7 and 8. Both probes were found to be water soluble and quenched intramolecularly via photoinduced electron transfer (PET) resulting in minimal background fluorescence. Upon incubating with Hint1, compound 7 and 8 exhibited a 40- and 16-fold increase in the fluorescence intensity compared to the control. Compounds 7 and 8 bind Hint1 with a dissociation constant of 0.121 ± 0.02 and 2.2 ± 0.36 µM, respectively. We demonstrate that probe 8 exhibits a switch-on FRET property with an active site tryptophan residue (W123). We show the utility of probes in performing quantitative ligand displacement studies, as well as in selective detection of Hint1 in the cell lysates. These probes should be useful for studying the dynamics of the active site, as well as for the development of fluorescence lifetime based high throughput screening assay to identify novel inhibitors for Hint1 in future.
[Mh] Termos MeSH primário: Transferência Ressonante de Energia de Fluorescência
Fluorescência
Corantes Fluorescentes/química
Proteínas do Tecido Nervoso/química
Neuralgia/tratamento farmacológico
Receptores Opioides/metabolismo
[Mh] Termos MeSH secundário: Sítios de Ligação
Corantes Fluorescentes/síntese química
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fluorescent Dyes); 0 (HINT1 protein, human); 0 (Nerve Tissue Proteins); 0 (Receptors, Opioid)
[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:171128
[St] Status:MEDLINE
[do] DOI:10.1039/c7ob02472j



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