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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


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[PMID]:27775688
[Au] Autor:Nomura A; Majumder K; Giri B; Dauer P; Dudeja V; Roy S; Banerjee S; Saluja AK
[Ad] Endereço:Division of Surgical Oncology, Department of Surgery Sylvester Comprehensive Cancer Center, University of Miami, Miami, FL, USA.
[Ti] Título:Inhibition of NF-kappa B pathway leads to deregulation of epithelial-mesenchymal transition and neural invasion in pancreatic cancer.
[So] Source:Lab Invest;96(12):1268-1278, 2016 12.
[Is] ISSN:1530-0307
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NF-κB has an essential role in the initiation and progression of pancreatic cancer and specifically mediates the induction of epithelial-mesenchymal transition and invasiveness. In this study, we demonstrate the importance of activated NF-κB signaling in EMT induction, lymphovascular metastasis, and neural invasion. Modulation of NF-κB activity was accomplished through the specific NF-κB inhibitor (BAY 11-7085), triptolide, and Minnelide treatment, as well as overexpression of IKBα repressor and IKK activator plasmids. In the classical lymphovascular metastatic cascade, inhibition of NF-κB decreased the expression of several EMT transcription factors (SNAI1, SNAI2, and ZEB1) and mesenchymal markers (VIM and CDH2) and decreased in vitro invasion, which was rescued by IKK activation. This was further demonstrated in vivo via BAY 11-7085 treatment in a orthotopic model of pancreatic cancer. In vivo NF-κB inhibition decreased tumor volume; decreased tumor EMT gene expression, while restoring cell-cell junctions; and decreasing overall metastasis. Furthermore, we demonstrate the importance of active NF-κB signaling in neural invasion. Triptolide treatment inhibits Nerve Growth Factor (NGF) mediated, neural-tumor co-culture in vitro invasion, and dorsal root ganglia (DRG) neural outgrowth through a disruption in tumor-neural cross talk. In vivo, Minnelide treatment decreased neurotrophin expression, nerve density, and sciatic nerve invasion. Taken together, this study demonstrates the importance of NF-κB signaling in the progression of pancreatic cancer through the modulation of EMT induction, lymphovascular invasion, and neural invasion.
[Mh] Termos MeSH primário: Transição Epitelial-Mesenquimal
NF-kappa B/metabolismo
Pâncreas/metabolismo
Neoplasias Pancreáticas/metabolismo
Nervos Periféricos/metabolismo
Neoplasias do Sistema Nervoso Periférico/secundário
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
Linhagem Celular
Linhagem Celular Tumoral
Técnicas de Cocultura
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Gânglios Espinais/citologia
Gânglios Espinais/efeitos dos fármacos
Gânglios Espinais/metabolismo
Gânglios Espinais/patologia
Seres Humanos
Metástase Linfática/patologia
Metástase Linfática/prevenção & controle
Camundongos
Camundongos Nus
Inibidor de NF-kappaB alfa/genética
Inibidor de NF-kappaB alfa/metabolismo
NF-kappa B/antagonistas & inibidores
Invasividade Neoplásica/patologia
Transplante de Neoplasias
Pâncreas/efeitos dos fármacos
Pâncreas/patologia
Neoplasias Pancreáticas/tratamento farmacológico
Neoplasias Pancreáticas/patologia
Nervos Periféricos/citologia
Nervos Periféricos/efeitos dos fármacos
Nervos Periféricos/patologia
Neoplasias do Sistema Nervoso Periférico/metabolismo
Neoplasias do Sistema Nervoso Periférico/patologia
Neoplasias do Sistema Nervoso Periférico/prevenção & controle
Proteínas Recombinantes/metabolismo
Nervo Isquiático/citologia
Nervo Isquiático/efeitos dos fármacos
Nervo Isquiático/metabolismo
Nervo Isquiático/patologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (NF-kappa B); 0 (Recombinant Proteins); 139874-52-5 (NF-KappaB Inhibitor alpha)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1038/labinvest.2016.109


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[PMID]:29358641
[Au] Autor:Qian Y; Zhao X; Han Q; Chen W; Li H; Yuan W
[Ad] Endereço:School of Pharmacy, Shanghai Jiao Tong University, 800 Dongchuan Road, Shanghai, 200240, China.
[Ti] Título:An integrated multi-layer 3D-fabrication of PDA/RGD coated graphene loaded PCL nanoscaffold for peripheral nerve restoration.
[So] Source:Nat Commun;9(1):323, 2018 01 22.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:As a conductive nanomaterial, graphene has huge potentials in nerve function restoration by promoting electrical signal transduction and metabolic activities with unique topological properties. Polydopamine (PDA) and arginylglycylaspartic acid (RGD) can improve cell adhesion in tissue engineering. Here we report an integrated 3D printing and layer-by-layer casting (LBLC) method in multi-layered porous scaffold fabrication. The scaffold is composed of single-layered graphene (SG) or multi-layered graphene (MG) and polycaprolactone (PCL). The electrically conductive 3D graphene scaffold can significantly improve neural expression both in vitro and in vivo. It promotes successful axonal regrowth and remyelination after peripheral nerve injury. These findings implicate that graphene-based nanotechnology have great potentials in peripheral nerve restoration in preclinical and clinical application.
[Mh] Termos MeSH primário: Materiais Biocompatíveis/química
Grafite/química
Indóis/química
Regeneração Nervosa/efeitos dos fármacos
Oligopeptídeos/química
Polímeros/química
Engenharia Tecidual/métodos
Tecidos Suporte
[Mh] Termos MeSH secundário: Animais
Materiais Biocompatíveis/farmacologia
Adesão Celular/efeitos dos fármacos
Condutividade Elétrica
Grafite/farmacologia
Indóis/farmacologia
Masculino
Teste de Materiais
Nanotecnologia/métodos
Regeneração Nervosa/fisiologia
Oligopeptídeos/farmacologia
Traumatismos dos Nervos Periféricos/patologia
Traumatismos dos Nervos Periféricos/fisiopatologia
Traumatismos dos Nervos Periféricos/reabilitação
Poliésteres/química
Poliésteres/farmacologia
Polímeros/farmacologia
Porosidade
Cultura Primária de Células
Impressão Tridimensional
Ratos
Ratos Sprague-Dawley
Células de Schwann/citologia
Células de Schwann/efeitos dos fármacos
Células de Schwann/fisiologia
Nervo Isquiático/efeitos dos fármacos
Nervo Isquiático/lesões
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biocompatible Materials); 0 (Indoles); 0 (Oligopeptides); 0 (Polyesters); 0 (Polymers); 0 (polydopamine); 24980-41-4 (polycaprolactone); 7782-42-5 (Graphite); 78VO7F77PN (arginyl-glycyl-aspartic acid)
[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:180124
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02598-7


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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]: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]:29307828
[Au] Autor:Wang X; Min S; Xie F; Yang J; Li L; Chen J
[Ad] Endereço:Department of Anesthesiology, First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
[Ti] Título:Glial cell-derived neurotrophic factor alleviates sepsis-induced neuromuscular dysfunction by decreasing the expression of γ- and α7-nicotinic acetylcholine receptors in an experimental rat model of neuromyopathy.
[So] Source:Biochem Biophys Res Commun;496(2):260-266, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sepsis-induced neuromuscular dysfunction results from up-regulation of the expression of γ- and α7-nicotinic acetylcholine receptors (nAChR). Although glial cell derived neurotrophic factor (GDNF) has been implicated in repairing and supporting neurons, little is known about the effects of GDNF on demyelination of nerves in sepsis. In this study, we tested the hypothesis that GDNF could alleviate sepsis-induced neuromuscular dysfunction by decreasing the expression of γ- and α7-nAChR in an experimental rat model of neuromyopathy. Rats were randomly divided into a sham group and a sepsis group. Levels of inflammatory factors, muscle function, and nicotinic acetylcholine receptors were tested in rats after cecal ligation and puncture (CLP). At 24 h after CLP, GDNF was injected around the sciatic nerve of sepsis rats, cytokines were detected by enzyme-linked immunosorbent assay (ELISA), and immunofluorescence staining was used to detect the expression of nAChRs. GDNF and its downstream effector (Erk1/2 and GFR-α), neuregulin-1 (NRG-1) and γ- and α7-nAChR were measured using Western blot analysis. The expression of GDNF reached a minimum at 24 h after CLP. Compared with the sham group, the release of cytokines and the expression of γ- and α7-nAChR were significantly increased in the sepsis group. The administration of GDNF significantly alleviated sepsis-induced neuromuscular dysfunction, as well as reducing the expression of γ- and α7-nAChR. In addition, the expression of Erk1/2, GFR-α, NRG-1 were significantly increased after GDNF treatment. GDNF administration may improve patient outcomes by reducing the demyelination of nerves and the expression of γ- and α7-nAChR.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Doenças Desmielinizantes/tratamento farmacológico
Fator Neurotrófico Derivado de Linhagem de Célula Glial/farmacologia
Doenças Musculares/tratamento farmacológico
Fármacos Neuroprotetores/farmacologia
Sepse/tratamento farmacológico
Receptor Nicotínico de Acetilcolina alfa7/genética
[Mh] Termos MeSH secundário: Animais
Citocinas/genética
Citocinas/metabolismo
Doenças Desmielinizantes/genética
Doenças Desmielinizantes/metabolismo
Doenças Desmielinizantes/patologia
Modelos Animais de Doenças
Regulação da Expressão Gênica
Fatores de Troca do Nucleotídeo Guanina/genética
Fatores de Troca do Nucleotídeo Guanina/metabolismo
Masculino
Proteína Quinase 1 Ativada por Mitógeno/genética
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/genética
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Doenças Musculares/genética
Doenças Musculares/metabolismo
Doenças Musculares/patologia
Neuregulina-1/genética
Neuregulina-1/metabolismo
Junção Neuromuscular/efeitos dos fármacos
Junção Neuromuscular/metabolismo
Junção Neuromuscular/patologia
Isoformas de Proteínas/antagonistas & inibidores
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Ratos
Ratos Sprague-Dawley
Nervo Isquiático/efeitos dos fármacos
Nervo Isquiático/metabolismo
Nervo Isquiático/patologia
Sepse/genética
Sepse/metabolismo
Sepse/patologia
Transdução de Sinais
Receptor Nicotínico de Acetilcolina alfa7/antagonistas & inibidores
Receptor Nicotínico de Acetilcolina alfa7/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (Guanine Nucleotide Exchange Factors); 0 (Neuregulin-1); 0 (Neuroprotective Agents); 0 (Nrg1 protein, rat); 0 (Protein Isoforms); 0 (alpha7 Nicotinic Acetylcholine Receptor); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE


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[PMID]:29025656
[Au] Autor:Xia B; Lv Y
[Ad] Endereço:Key Laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education, Bioengineering College, Chongqing University, Chongqing 400044, PR China; Mechanobiology and Regenerative Medicine Laboratory, Bioengineering College, Chongqing University, Chongqing 400044, PR China.
[Ti] Título:Dual-delivery of VEGF and NGF by emulsion electrospun nanofibrous scaffold for peripheral nerve regeneration.
[So] Source:Mater Sci Eng C Mater Biol Appl;82:253-264, 2018 Jan 01.
[Is] ISSN:1873-0191
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Controlled delivery of multiple therapeutic agents can be considered an effective approach in nerve injury due to its multifunction. In this study, recombinant human vascular endothelial growth factor (VEGF) and recombinant human nerve growth factor (NGF) were loaded on the surface and in the core of emulsion electrospun poly (l-lactic acid) (PLLA) nanofibrous scaffold, respectively. The in vitro studies showed that VEGF and NGF had a sequential release pattern in which most of the VEFG was released in the first few days but the NGF could be continuously released for >1month. The dual-delivery scaffold could enhance the neural differentiation of induced pluripotent stem cells-derived neural crest stem cells (iPSCs-NCSCs) in vitro. Furthermore, this scaffold was applied to a critical sized defect in rat sciatic nerve model. Footprint analysis, electrophysiological tests, and histological analysis revealed that a significant improvement of neovascularization as well as nerve healing after 3months post-operation could be achieved by dual-delivery of VEGF and NGF. Taken together, the present study indicated that VEGF and NGF in emulsion electrospun nanofibrous scaffold had a synergistic effect on regeneration of vascularized nerve tissue.
[Mh] Termos MeSH primário: Emulsões/química
Nanofibras/química
Fator de Crescimento Neural/química
Nervo Isquiático/fisiologia
Tecidos Suporte/química
Fator A de Crescimento do Endotélio Vascular/química
[Mh] Termos MeSH secundário: Animais
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Feminino
Expressão Gênica/efeitos dos fármacos
Proteína Glial Fibrilar Ácida/genética
Proteína Glial Fibrilar Ácida/metabolismo
Células-Tronco Pluripotentes Induzidas/citologia
Células-Tronco Pluripotentes Induzidas/metabolismo
Proteínas Associadas aos Microtúbulos/genética
Proteínas Associadas aos Microtúbulos/metabolismo
Fator de Crescimento Neural/farmacologia
Regeneração Nervosa/efeitos dos fármacos
Células-Tronco Neurais/citologia
Células-Tronco Neurais/metabolismo
Poliésteres/química
Ratos
Ratos Sprague-Dawley
Recuperação de Função Fisiológica
Nervo Isquiático/patologia
Fator A de Crescimento do Endotélio Vascular/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Emulsions); 0 (Glial Fibrillary Acidic Protein); 0 (Microtubule-Associated Proteins); 0 (Polyesters); 0 (Vascular Endothelial Growth Factor A); 459TN2L5F5 (poly(lactide)); 9061-61-4 (Nerve Growth Factor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE


  8 / 17479 MEDLINE  
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[PMID]:29224279
[Au] Autor:Bai J; Zhang Y; Wang YF; Lan J; Li XQ
[Ad] Endereço:Department of Pathophysiology, Shanxi Medical University, Taiyuan 030001, China.
[Ti] Título:[Overexpression of TRPV1 after periphery nerve injury attenuates nerve regeneration in rats].
[So] Source:Zhonghua Bing Li Xue Za Zhi;46(12):847-852, 2017 Dec 08.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To observe the effect of the expressive or functional blockage of TRPV1 on nerve regeneration after sciatic trans-section injury. AMG-517, a kind of TRPV1 inhibitor, was injected into the surrounding area of the ipsilateral lumbar dorsal root ganglia while unilateral sciatic nerve was transected. A total of 24 healthy male Sprague-Dawley rats were divided into 4 groups: control group, injury only group, injury+ AMG-517 150 µg/kg group, injury+ AMG-517 300 µg/kg group. The injury only group was injected the same volume of medium. The release of CGRP from dorsal-horn of spinal cord, the number of axons at proximal stem of sciatic nerve after transection, and the expression of TRPV1 in dorsal root ganglion were detected using the methods of ELISA, Western blot and semi-thin section (1 µm)- toluidine blue staining 2 weeks after injury. The release of CGRP in lumbar spinal dorsal horn was obviously decreased after AMG-517 treatment, which was the evidence of TRPV1 functional inhibition. CGRP in the control group was 0.15 ng/g, the injury only group 0.17 ng/g, AMG-517 150 µg/kg group 0.09 ng/g, and AMG-517 300 µg/kg group 0.11 ng/g( <0.01). The number of axons which were myelinated or unmyelinated increased after the TRPV1 was inhibited by AMG-517( <0.01). In addition, the injection of AMG-517 into surrounding dorsal root ganglion decreased the expression of TRPV1 in dorsal root ganglion( <0.01). Over expression or activation of TRPV1 after periphery nerve injury has negative effect on nerve regeneration in fact; Inhibiting the over-expression or over-activation of TRPV1 after nerve injury facilitates axonal regeneration and nerve repair.
[Mh] Termos MeSH primário: Regeneração Nervosa
Nervo Isquiático/lesões
Canais de Cátion TRPV/metabolismo
[Mh] Termos MeSH secundário: Animais
Axônios
Benzotiazóis/farmacologia
Gânglios Espinais/efeitos dos fármacos
Gânglios Espinais/metabolismo
Masculino
Pirimidinas/farmacologia
Ratos
Ratos Sprague-Dawley
Medula Espinal
Canais de Cátion TRPV/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzothiazoles); 0 (N-(4-(6-(4-trifluoromethylphenyl)pyrimidin-4-yloxy)benzothiazol-2-yl)acetamide); 0 (Pyrimidines); 0 (TRPV Cation Channels); 0 (Trpv1 protein, rat)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2017.12.007


  9 / 17479 MEDLINE  
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[PMID]:28452816
[Au] Autor:Santamaria CM; Zhan C; McAlvin JB; Zurakowski D; Kohane DS
[Ad] Endereço:From the *Laboratory for Biomaterials and Drug Delivery, Division of Critical Care Medicine, Department of Anesthesiology; †Division of Medicine Critical Care, Department of Medicine; and ‡Department of Anesthesiology, Perioperative, and Pain Medicine, Boston Children's Hospital, Boston, Massachusetts.
[Ti] Título:Tetrodotoxin, Epinephrine, and Chemical Permeation Enhancer Combinations in Peripheral Nerve Blockade.
[So] Source:Anesth Analg;124(6):1804-1812, 2017 06.
[Is] ISSN:1526-7598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Chemical permeation enhancers (CPEs) have the potential to improve nerve blockade by site 1 sodium channel blockers such as tetrodotoxin (TTX). Here, we investigated the efficacy and toxicity of CPE-enhanced nerve blockade across a range of TTX concentrations using 2 CPEs (sodium octyl sulfate and octyl trimethyl ammonium bromide). We also tested the hypothesis that CPEs could be used to reduce the concentrations of TTX and/or of a second adjuvant drug (in this case, epinephrine) needed to achieve prolonged local anesthesia METHODS:: Sprague-Dawley rats were injected at the sciatic nerve with combinations of TTX and CPEs, with and without epinephrine. Sensory and motor nerve blockade were assessed using a modified hot plate test and a weight-bearing test, respectively. Systemic and local toxicities of the different combinations were assessed. RESULTS: Addition of increasing concentrations of TTX to fixed concentrations of CPEs produced a marked concentration-dependent improvement in the rate of successful nerve blocks and in nerve block duration. CPEs did not affect systemic toxicity. At some concentrations, the addition of sodium octyl sulfate increased the duration of block from TTX plus epinephrine, and epinephrine increased that from TTX plus CPEs. The addition of epinephrine did not cause an increase in local toxicity, and it markedly reduced systemic toxicity. CONCLUSIONS: CPEs can prolong the duration of nerve blockade across a range of concentrations of TTX. CPEs could also be used to reduce the concentration of epinephrine needed to achieve a given degree of nerve block. CPEs may be useful in enhancing nerve blockade from site 1 sodium channel blockers.
[Mh] Termos MeSH primário: Agonistas Adrenérgicos/farmacologia
Ácidos Alcanossulfônicos/farmacologia
Anestésicos Locais/farmacologia
Epinefrina/farmacologia
Bloqueio Nervoso/métodos
Compostos de Amônio Quaternário/farmacologia
Nervo Isquiático/efeitos dos fármacos
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
[Mh] Termos MeSH secundário: Agonistas Adrenérgicos/toxicidade
Anestésicos Locais/toxicidade
Animais
Difusão
Relação Dose-Resposta a Droga
Epinefrina/toxicidade
Masculino
Atividade Motora/efeitos dos fármacos
Bloqueio Nervoso/efeitos adversos
Limiar da Dor/efeitos dos fármacos
Permeabilidade
Ratos Sprague-Dawley
Bloqueadores dos Canais de Sódio/toxicidade
Tetrodotoxina/toxicidade
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Adrenergic Agonists); 0 (Alkanesulfonic Acids); 0 (Anesthetics, Local); 0 (Quaternary Ammonium Compounds); 0 (Sodium Channel Blockers); 15461-38-8 (octyltrimethylammonium); 4368-28-9 (Tetrodotoxin); DU4821I15A (1-octanesulfonic acid); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1213/ANE.0000000000002072


  10 / 17479 MEDLINE  
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[PMID]:27770818
[Au] Autor:Altmann C; Vasic V; Hardt S; Heidler J; Häussler A; Wittig I; Schmidt MH; Tegeder I
[Ad] Endereço:Institute of Clinical Pharmacology, Goethe-University Hospital, Frankfurt, Germany.
[Ti] Título:Progranulin promotes peripheral nerve regeneration and reinnervation: role of notch signaling.
[So] Source:Mol Neurodegener;11(1):69, 2016 10 22.
[Is] ISSN:1750-1326
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Peripheral nerve injury is a frequent cause of lasting motor deficits and chronic pain. Although peripheral nerves are capable of regrowth they often fail to re-innervate target tissues. RESULTS: Using newly generated transgenic mice with inducible neuronal progranulin overexpression we show that progranulin accelerates axonal regrowth, restoration of neuromuscular synapses and recovery of sensory and motor functions after injury of the sciatic nerve. Oppositely, progranulin deficient mice have long-lasting deficits in motor function tests after nerve injury due to enhanced losses of motor neurons and stronger microglia activation in the ventral horn of the spinal cord. Deep proteome and gene ontology (GO) enrichment analysis revealed that the proteins upregulated in progranulin overexpressing mice were involved in 'regulation of transcription' and 'response to insulin' (GO terms). Transcription factor prediction pointed to activation of Notch signaling and indeed, co-immunoprecipitation studies revealed that progranulin bound to the extracellular domain of Notch receptors, and this was functionally associated with higher expression of Notch target genes in the dorsal root ganglia of transgenic mice with neuronal progranulin overexpression. Functionally, these transgenic mice recovered normal gait and running, which was not achieved by controls and was stronger impaired in progranulin deficient mice. CONCLUSION: We infer that progranulin activates Notch signaling pathways, enhancing thereby the regenerative capacity of partially injured neurons, which leads to improved motor function recovery.
[Mh] Termos MeSH primário: Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Regeneração Nervosa/fisiologia
Traumatismos dos Nervos Periféricos/metabolismo
Receptores Notch/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Modelos Animais de Doenças
Ensaio de Imunoadsorção Enzimática
Feminino
Imunoprecipitação
Hibridização in Situ Fluorescente
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Reação em Cadeia da Polimerase em Tempo Real
Recuperação de Função Fisiológica/fisiologia
Nervo Isquiático/lesões
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Grn protein, mouse); 0 (Intercellular Signaling Peptides and Proteins); 0 (Receptors, Notch)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171211
[Lr] Data última revisão:
171211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE



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