Base de dados : MEDLINE
Pesquisa : D12.776.395.550.400 [Categoria DeCS]
Referências encontradas : 2254 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 226 ir para página                         

  1 / 2254 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29273038
[Au] Autor:Villareal MO; Ikeya A; Sasaki K; Arfa AB; Neffati M; Isoda H
[Ad] Endereço:Faculty of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba City, Ibaraki, 305-8572, Japan.
[Ti] Título:Anti-stress and neuronal cell differentiation induction effects of Rosmarinus officinalis L. essential oil.
[So] Source:BMC Complement Altern Med;17(1):549, 2017 Dec 22.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mood disorder accounts for 13 % of global disease burden. And while therapeutic agents are available, usually orally administered, most have unwanted side effects, and thus making the inhalation of essential oils (EOs) an attractive alternative therapy. Rosmarinus officinalis EO (ROEO), Mediterranean ROEO reported to improve cognition, mood, and memory, the effect on stress of which has not yet been determined. Here, the anti-stress effect of ROEO on stress was evaluated in vivo and in vitro. METHODS: Six-week-old male ICR mice were made to inhale ROEO and subjected to tail suspension test (TST). To determine the neuronal differentiation effect of ROEO in vitro, induction of ROEO-treated PC12 cells differentiation was observed. Intracellular acetylcholine and choline, as well as the Gap43 gene expression levels were also determined. RESULTS: Inhalation of ROEO significantly decreased the immobility time of ICR mice and serum corticosterone level, accompanied by increased brain dopamine level. Determination of the underlying mechanism in vitro revealed a PC12 differentiation-induction effect through the modulation of intracellular acetylcholine, choline, and Gap43 gene expression levels. ROEO activates the stress response system through the NGF pathway and the hypothalamus-pituitary-adrenal axis, promoting dopamine production and secretion. The effect of ROEO may be attributed to its bioactive components, specifically to α-pinene, one of its major compounds that has anxiolytic property. CONCLUSIONS: The results of this study suggest that ROEO inhalation has therapeutic potential against stress-related psychiatric disorders.
[Mh] Termos MeSH primário: Química Encefálica/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Óleos Voláteis/farmacologia
Rosmarinus
Estresse Psicológico/metabolismo
[Mh] Termos MeSH secundário: Acetilcolinesterase/metabolismo
Animais
Comportamento Animal/efeitos dos fármacos
Catecolaminas/metabolismo
Proteína GAP-43/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos ICR
Células PC12
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Catecholamines); 0 (GAP-43 Protein); 0 (Oils, Volatile); 8LGU7VM393 (rosemary oil); EC 3.1.1.7 (Acetylcholinesterase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171224
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-2060-1


  2 / 2254 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29176876
[Au] Autor:Stifter J; Ulbrich F; Goebel U; Böhringer D; Lagrèze WA; Biermann J
[Ad] Endereço:Eye Center, Medical Center-University of Freiburg, Killianstrasse 5, Freiburg, Germany.
[Ti] Título:Neuroprotection and neuroregeneration of retinal ganglion cells after intravitreal carbon monoxide release.
[So] Source:PLoS One;12(11):e0188444, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Retinal ischemia induces apoptosis leading to neurodegeneration and vision impairment. Carbon monoxide (CO) in gaseous form showed cell-protective and anti-inflammatory effects after retinal ischemia-reperfusion-injury (IRI). These effects were also demonstrated for the intravenously administered CO-releasing molecule (CORM) ALF-186. This article summarizes the results of intravitreally released CO to assess its suitability as a neuroprotective and neuroregenerative agent. METHODS: Water-soluble CORM ALF-186 (25 µg), PBS, or inactivated ALF (iALF) (all 5 µl) were intravitreally applied into the left eyes of rats directly after retinal IRI for 1 h. Their right eyes remained unaffected and were used for comparison. Retinal tissue was harvested 24 h after intervention to analyze mRNA or protein expression of Caspase-3, pERK1/2, p38, HSP70/90, NF-kappaB, AIF-1 (allograft inflammatory factor), TNF-α, and GAP-43. Densities of fluorogold-prelabeled retinal ganglion cells (RGC) were examined in flat-mounted retinae seven days after IRI and were expressed as mean/mm2. The ability of RGC to regenerate their axon was evaluated two and seven days after IRI using retinal explants in laminin-1-coated cultures. Immunohistochemistry was used to analyze the different cell types growing out of the retinal explants. RESULTS: Compared to the RGC-density in the contralateral right eyes (2804±214 RGC/mm2; data are mean±SD), IRI+PBS injection resulted in a remarkable loss of RGC (1554±159 RGC/mm2), p<0.001. Intravitreally injected ALF-186 immediately after IRI provided RGC protection and reduced the extent of RGC-damage (IRI+PBS 1554±159 vs. IRI+ALF 2179±286, p<0.001). ALF-186 increased the IRI-mediated phosphorylation of MAP-kinase p38. Anti-apoptotic and anti-inflammatory effects were detectable as Caspase-3, NF-kappaB, TNF-α, and AIF-1 expression were significantly reduced after IRI+ALF in comparison to IRI+PBS or IRI+iALF. Gap-43 expression was significantly increased after IRI+ALF. iALF showed effects similar to PBS. The intrinsic regenerative potential of RGC-axons was induced to nearly identical levels after IRI and ALF or iALF-treatment under growth-permissive conditions, although RGC viability differed significantly in both groups. Intravitreal CO further increased the IRI-induced migration of GFAP-positive cells out of retinal explants and their transdifferentiation, which was detected by re-expression of beta-III tubulin and nestin. CONCLUSION: Intravitreal CORM ALF-186 protected RGC after IRI and stimulated their axons to regenerate in vitro. ALF conveyed anti-apoptotic, anti-inflammatory, and growth-associated signaling after IRI. CO's role in neuroregeneration and its effect on retinal glial cells needs further investigation.
[Mh] Termos MeSH primário: Monóxido de Carbono/metabolismo
Regeneração Nervosa
Neuroproteção
Células Ganglionares da Retina/metabolismo
[Mh] Termos MeSH secundário: Animais
Axônios/efeitos dos fármacos
Axônios/metabolismo
Proteínas de Ligação ao Cálcio/genética
Proteínas de Ligação ao Cálcio/metabolismo
Caspase 3/genética
Caspase 3/metabolismo
Movimento Celular/efeitos dos fármacos
Células Cultivadas
Complexos de Coordenação/administração & dosagem
Complexos de Coordenação/farmacologia
Complexos de Coordenação/uso terapêutico
Feminino
Proteína GAP-43/genética
Proteína GAP-43/metabolismo
Proteína Glial Fibrilar Ácida/metabolismo
Proteínas de Choque Térmico HSP70/metabolismo
Proteínas de Choque Térmico HSP90/metabolismo
Injeções Intravítreas
Masculino
Proteínas dos Microfilamentos/genética
Proteínas dos Microfilamentos/metabolismo
Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/genética
NF-kappa B/metabolismo
Regeneração Nervosa/efeitos dos fármacos
Neuroglia/efeitos dos fármacos
Neuroglia/metabolismo
Neuroproteção/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Fármacos Neuroprotetores/uso terapêutico
Fosforilação/efeitos dos fármacos
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos Sprague-Dawley
Traumatismo por Reperfusão/tratamento farmacológico
Traumatismo por Reperfusão/genética
Traumatismo por Reperfusão/patologia
Células Ganglionares da Retina/efeitos dos fármacos
Células Ganglionares da Retina/patologia
Tubulina (Proteína)/metabolismo
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, rat); 0 (Calcium-Binding Proteins); 0 (Coordination Complexes); 0 (GAP-43 Protein); 0 (Glial Fibrillary Acidic Protein); 0 (HSP70 Heat-Shock Proteins); 0 (HSP90 Heat-Shock Proteins); 0 (Microfilament Proteins); 0 (NF-kappa B); 0 (Neuroprotective Agents); 0 (RNA, Messenger); 0 (Tubb3 protein, rat); 0 (Tubulin); 0 (Tumor Necrosis Factor-alpha); 0 (triscarbonyl(histidinato)molybdate(III)); 7U1EE4V452 (Carbon Monoxide); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188444


  3 / 2254 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28796579
[Au] Autor:Jiang B; Zhang Y; Zhao J; She C; Zhou X; Dong Q; Wang P
[Ad] Endereço:a Department of Hand and Foot Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, P. R. China.
[Ti] Título:Effects of Localized X-Ray Irradiation on Peripheral Nerve Regeneration in Transected Sciatic Nerve in Rats.
[So] Source:Radiat Res;188(4):455-462, 2017 Oct.
[Is] ISSN:1938-5404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Low-dose radiation has been used in clinical and experimental models for the prevention of scarring and for fracture healing. There is evidence that low-dose radiation improves the hormesis of various cell types but little is known about its effects on peripheral nerve tissue. In this study, we investigated the beneficial effects of low-dose radiation on the regeneration of transectional peripheral nerve injury in an experimental rat model. Seventy-two male Sprague-Dawley rats received transection injury to the left sciatic nerves, and the nerves were subsequently sutured by epineurium end-to-end anastomosis to restore continuity. Animals were randomly assigned to one of two treatment groups (n = 36/group): 1 Gy X-ray irradiation or control (sham irradiation). Gait analysis, electrophysiological examination and morphological investigations were performed. In addition, Western blot and qRT-PCR were performed to determine the level of vascular endothelial growth factor (VEGF) and growth-associated protein-43 (GAP-43). Content of VEGF and GAP-43 in the regenerated sciatic nerve of the irradiated group was higher than the control group. At 4 to 12 weeks after surgery, the irradiated animals exhibited a significantly improved functional recovery relative to controls. At 12 weeks after surgery, amplitude and conduction velocity of the irradiated group were higher than the control group (P < 0.05). The number of nerve fibers, diameter of axons and morphological structure of the myelin sheath in the irradiated group were superior to those of the control group. These results suggest that low-dose radiation contributed to regeneration and functional recovery after transverse peripheral nerve injury by inducing increased production of VEGF and GAP-43, which promote the axonal regeneration and myelination.
[Mh] Termos MeSH primário: Regeneração Nervosa/efeitos da radiação
Nervo Isquiático/fisiologia
Nervo Isquiático/efeitos da radiação
Nervo Isquiático/cirurgia
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Fenômenos Eletrofisiológicos/efeitos da radiação
Proteína GAP-43/metabolismo
Masculino
Ratos
Ratos Sprague-Dawley
Recuperação de Função Fisiológica/efeitos da radiação
Nervo Isquiático/citologia
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GAP-43 Protein); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM; S
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1667/RR14799.1


  4 / 2254 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28535499
[Au] Autor:Lin W; Huang W; Chen S; Lin M; Huang Q; Huang H
[Ad] Endereço:Department of Neurology, Fujian Medical University Union Hospital, Fuzhou, China.
[Ti] Título:The Role of 5-HTR6 in Mossy Fiber Sprouting: Activating Fyn and p-ERK1/2 in Pilocarpine-Induced Chronic Epileptic Rats.
[So] Source:Cell Physiol Biochem;42(1):231-241, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Our primary objective is to verify whether 5-HTR6 is involved in the development of mossy fiber sprouting (MFS), and to determine how the progression of MFS is affected by 5-HTR6. METHODS: A total of 90 male adult Sprague-Dawley rats were allocated into either the control group (n=36) or the epileptic group (n=54). Status epilepticus (SE) of rats was induced by the intraperitoneal (i.p.) injection of LiCl-pilocarpine. We conducted our experiments in two stages. The first stage involves equally dividing 36 epileptic rats into three groups with treatments of none, 5-HTR6 antagonist SB-27104 (SB) and vehicle DMSO. Then behavior and electroencephalogram (EEG) of rats were monitored by video-EEG. The second stage involves dividing 126 epileptic rats into seven groups with treatments of none, 10% DMSO, SB (100 µg/kg), Fyn antagonist PP2 (50 µg/kg), p-ERK1/2 antagonist PD-98059 (30 µg/kg), SB (100 µg/ kg) + PP2 (50 µg/kg); SB (100 µg/kg) + PD-98059 (30 µg/kg). We also treated 18 rats in the control group of the first stage with 100 µg/kg 5-HTR6 agonist WAY-181187 (WAY). MFS of rats was detected through the approach of Timm's staining. Finally, expressions of 5-HTR6, Fyn, p-ERK1/2 and GAP-3 were qualified and semi-quantified via western blotting or RT-PCR. RESULTS: Induction of SE could stimulate formation of MFS and increased GAP-43 expressions. Expressions of 5-HTR6, Fyn and p-ERK1/2 were also up-regulated with increasing time after establishment of SE models. The development of MFS was remarkably inhibited by SB, PP2 and PD. Compared to the single antagonist, such an inhibitory effect was enhanced by SB+PD or SB+PP. Moreover, treatment of healthy rats with WAY would contribute to up-regulated Fyn and p-ERK1/2 expressions, as well as development of MFS (P < 0.05). Suppression of Fyn triggered a down-regulating trend of p-ERK1/2 (P < 0.05), however, suppressed p-ERK1/2 did not have such a significant effect on Fyn expression. CONCLUSION: HTR6 may affect the progression of MFS by activating both p-ERK1/2 and Fyn, which further modulate the expression of GAP-43.
[Mh] Termos MeSH primário: Epilepsia/fisiopatologia
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Proteínas Proto-Oncogênicas c-fyn/metabolismo
Receptores de Serotonina/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Epilepsia/induzido quimicamente
Flavonoides/farmacologia
Proteína GAP-43/genética
Proteína GAP-43/metabolismo
Masculino
Proteína Quinase 1 Ativada por Mitógeno/antagonistas & inibidores
Proteína Quinase 3 Ativada por Mitógeno/antagonistas & inibidores
Agonistas Muscarínicos/farmacologia
Pilocarpina/toxicidade
Proteínas Proto-Oncogênicas c-fyn/antagonistas & inibidores
RNA Mensageiro/metabolismo
Ratos
Ratos Sprague-Dawley
Receptores de Serotonina/química
Agonistas de Receptores de Serotonina/farmacologia
Estado Epiléptico/induzido quimicamente
Estado Epiléptico/patologia
Tiazóis/farmacologia
Fatores de Tempo
Triptaminas/farmacologia
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one); 0 (Flavonoids); 0 (GAP-43 Protein); 0 (Muscarinic Agonists); 0 (N(1)-(6-chloroimidazo(2,1-b)(1,3)thiazole-5-sulfonyl)tryptamine); 0 (RNA, Messenger); 0 (Receptors, Serotonin); 0 (Serotonin Receptor Agonists); 0 (Thiazoles); 0 (Tryptamines); 0 (serotonin 6 receptor); 01MI4Q9DI3 (Pilocarpine); EC 2.7.10.2 (Fyn protein, rat); EC 2.7.10.2 (Proto-Oncogene Proteins c-fyn); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE
[do] DOI:10.1159/000477322


  5 / 2254 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28505619
[Au] Autor:Cui J; Cui C; Cui Y; Li R; Sheng H; Jiang X; Tian Y; Wang K; Gao J
[Ad] Endereço:Department of Neurosurgery, Tangshan Gongren Hospital, Tangshan, China.
[Ti] Título:Bone Marrow Mesenchymal Stem Cell Transplantation Increases GAP-43 Expression via ERK1/2 and PI3K/Akt Pathways in Intracerebral Hemorrhage.
[So] Source:Cell Physiol Biochem;42(1):137-144, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Intracerebral hemorrhage (ICH) occurs in hypertensive patients and results in high rates of mortality and disability. This study determined whether bone marrow mesenchymal stem cell (BMSC) transplantation affects axonal regeneration and examined the underlying mechanisms after the administration of PD98059 (p-ERK1/2 inhibitor) or/ and LY294002 (PI3K inhibitor). The hypothesis that was intended to be tested was that BMSC transplantation regulates the expression of growth-associated protein-43 (GAP-43) via the ERK1/2 and PI3K/Akt signaling pathways. METHODS: Seventy-five male rats (250-280 g) were subjected to intracerebral blood injection and then randomly received a vehicle, BMSCs, PD98059 or LY294002 treatment. Neurological deficits were evaluated prior to injury and at 1, 3 and 7 days post-injury. The expression of GAP-43, Akt, p-Akt, ERK1/2, and p-ERK1/2 proteins was measured by western blot analysis. RESULTS: BMSC transplantation attenuated neurological deficits 3-7 days post-ICH. The expression of GAP-43 was increased 3 days following BMSC transplantation. However, this increase was inhibited by either PD98059 or LY294002 treatment. Treatment with both PD98059 and LY294002 was more effective than was treatment with an individual compound. CONCLUSION: BMSC transplantation could attenuate neurological deficits and activate axonal regeneration in this rat ICH model. The protective effects might be associated with increased GAP-43 expression by activating both the ERK1/2 and PI3K/Akt signaling pathways.
[Mh] Termos MeSH primário: Hemorragia Cerebral/terapia
Proteína GAP-43/metabolismo
Transplante de Células-Tronco Mesenquimais
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Axônios/fisiologia
Células da Medula Óssea/citologia
Células Cultivadas
Hemorragia Cerebral/induzido quimicamente
Hemorragia Cerebral/patologia
Cromonas/farmacologia
Modelos Animais de Doenças
Flavonoides/farmacologia
Masculino
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/metabolismo
Proteína Quinase 1 Ativada por Mitógeno/antagonistas & inibidores
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/antagonistas & inibidores
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Morfolinas/farmacologia
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Ratos
Ratos Sprague-Dawley
Regeneração
Transdução de Sinais/efeitos dos fármacos
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one); 0 (Chromones); 0 (Flavonoids); 0 (GAP-43 Protein); 0 (Morpholines); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170516
[St] Status:MEDLINE
[do] DOI:10.1159/000477122


  6 / 2254 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28394221
[Au] Autor:Yuan Q; Sun L; Yu H; An C
[Ad] Endereço:a Department of Orthopedics , Shengjing Hospital of China Medical University , Shenyang , People's Republic of China.
[Ti] Título:Human microvascular endothelial cell promotes the development of dorsal root ganglion neurons via BDNF pathway in a co-culture system.
[So] Source:Biosci Biotechnol Biochem;81(7):1335-1342, 2017 Jul.
[Is] ISSN:1347-6947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Our previous study found that co-culture with human vascular endothelial cells (HMVECs) is beneficial for dorsal root ganglion cells (DRGCs). The goal of the present study is to investigate whether co-culture with HMVECs could promote the development of DRGCs, and whether this effect is induced by the secretion of BDNF by HMVECs. DRGCs were mono-cultured, co-cultured with HMVECs or co-cultured with HMVECs that pre-transfected with BDNF siRNA, the expression of neurite formation and branching factors were determined. The results showed that transfecting with BDNF siRNA inhibited BDNF expression and reduced BDNF secretion. Co-culture with HMVECs increased the expression of Etv4, Etv5, FN-L, FN-M, and GAP-43 in DRGCs that accompanied by the activation of ERK pathway. However, these changes were all reversed by the inhibition of BDNF in HMVECs. In conclusion, our data demonstrate that HMVECs potentiated DRGCs development at least partly by the secretion of BDNF in the co-culture system.
[Mh] Termos MeSH primário: Fator Neurotrófico Derivado do Encéfalo/genética
Células Endoteliais/metabolismo
Gânglios Espinais/metabolismo
Neurônios/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Fator Neurotrófico Derivado do Encéfalo/antagonistas & inibidores
Fator Neurotrófico Derivado do Encéfalo/secreção
Comunicação Celular
Diferenciação Celular
Linhagem Celular
Técnicas de Cocultura
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Células Endoteliais/citologia
Proteína GAP-43/genética
Proteína GAP-43/metabolismo
Gânglios Espinais/citologia
Regulação da Expressão Gênica
Seres Humanos
Camundongos
Neurônios/citologia
Cultura Primária de Células
Proteínas Proto-Oncogênicas c-ets/genética
Proteínas Proto-Oncogênicas c-ets/metabolismo
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (DNA-Binding Proteins); 0 (Etv4 protein, mouse); 0 (Etv5 protein, mouse); 0 (GAP-43 Protein); 0 (Proto-Oncogene Proteins c-ets); 0 (RNA, Small Interfering); 0 (Transcription Factors); 0 (brain-derived neurotrophic factor, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170707
[Lr] Data última revisão:
170707
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.1080/09168451.2017.1313695


  7 / 2254 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28385489
[Au] Autor:Christen V; Rusconi M; Crettaz P; Fent K
[Ad] Endereço:University of Applied Sciences and Arts Northwestern Switzerland, School of Life Sciences, Gründenstrasse 40, CH-4132, Muttenz, Switzerland.
[Ti] Título:Developmental neurotoxicity of different pesticides in PC-12 cells in vitro.
[So] Source:Toxicol Appl Pharmacol;325:25-36, 2017 Jun 15.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The detection of developmental neurotoxicity (DNT) of chemicals has high relevance for protection of human health. However, DNT of many pesticides is only little known. Furthermore, validated in vitro systems for assessment of DNT are not well established. Here we employed the rat phaeochromocytoma cell line PC-12 to evaluate DNT of 18 frequently used pesticides of different classes, including neonicotinoids, pyrethroids, organophosphates, organochlorines, as well as quaternary ammonium compounds, the organic compound used in pesticides, piperonyl butoxide, as well as the insect repellent diethyltoluamide (DEET). We determined the outgrowth of neurites in PC-12 cells co-treated with nerve growth factor and different concentrations of biocides for 5days. Furthermore, we determined transcriptional alterations of selected genes that may be associated with DNT, such as camk2α and camk2ß, gap-43, neurofilament-h, tubulin-α and tubulin-ß. Strong and dose- dependent inhibition of neurite outgrowth was induced by azamethiphos and chlorpyrifos, and dieldrin and heptachlor, which was correlated with up-regulation of gap-43. No or only weak effects on neurite outgrowth and transcriptional alterations occurred for neonicotinoids acetamiprid, clothianidin, imidacloprid and thiamethoxam, the pyrethroids λ-cyhalothrin, cyfluthrin, deltamethrin, and permethrin, the biocidal disinfectants C12-C14-alkyl(ethylbenzyl)dimethylammonium (BAC), benzalkonium chloride and barquat (dimethyl benzyl ammonium chloride), and piperonyl butoxide and DEET. Our study confirms potential developmental neurotoxicity of some pesticides and provides first evidence that azamethiphos has the potential to act as a developmental neurotoxic compound. We also demonstrate that inhibition of neurite outgrowth and transcriptional alterations of gap-43 expression correlate, which suggests the employment of gap-43 expression as a biomarker for detection and initial evaluation of potential DNT of chemicals.
[Mh] Termos MeSH primário: Neurogênese/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Síndromes Neurotóxicas/etiologia
Praguicidas/toxicidade
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Proteína GAP-43/genética
Proteína GAP-43/metabolismo
Marcadores Genéticos
Neuritos/efeitos dos fármacos
Neuritos/metabolismo
Neuritos/patologia
Neurônios/metabolismo
Neurônios/patologia
Síndromes Neurotóxicas/metabolismo
Síndromes Neurotóxicas/patologia
Células PC12
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos
Medição de Risco
Fatores de Tempo
Testes de Toxicidade
Transcrição Genética/efeitos dos fármacos
Ativação Transcricional/efeitos dos fármacos
Regulação para Cima
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GAP-43 Protein); 0 (Genetic Markers); 0 (Pesticides); 0 (RNA, Messenger)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170530
[Lr] Data última revisão:
170530
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170408
[St] Status:MEDLINE


  8 / 2254 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
[PMID]:28380213
[Au] Autor:Li Y; Gao X; Wang Q; Yang Y; Liu H; Zhang B; Li L
[Ad] Endereço:Department of Geriatrics, Southern Medical University Zhu Jiang Hospital, Guangzhou, China.
[Ti] Título:Retinoic acid protects from experimental cerebral infarction by upregulating GAP-43 expression.
[So] Source:Braz J Med Biol Res;50(4):e5561, 2017 Apr 03.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to investigate whether exogenous retinoic acid (RA) can upregulate the mRNA and protein expression of growth-associated protein 43 (GAP-43), thereby promoting brain functional recovery in a rat distal middle cerebral artery occlusion (MCAO) model of ischemia. A total of 216 male Sprague Dawley rats weighing 300-320 g were divided into 3 groups: sham-operated group, MCAO+vehicle group and MCAO+RA group. Focal cortical infarction was induced with a distal MCAO model. The expression of GAP-43 mRNA and protein in the ipsilateral perifocal region was assessed using qPCR and immunocytochemistry at 1, 3, 7, 14, 21, and 28 days after distal MCAO. In addition, an intraperitoneal injection of RA was given 12 h before MCAO and continued every day until the animal was sacrificed. Following ischemia, the expression of GAP-43 first increased considerably and then decreased. Administration of RA reduced infarction volume, promoted neurological functional recovery and upregulated expression of GAP-43. Administration of RA can ameliorate neuronal damage and promote nerve regeneration by upregulating the expression of GAP-43 in the perifocal region after distal MCAO.
[Mh] Termos MeSH primário: Proteína GAP-43/metabolismo
Expressão Gênica/efeitos dos fármacos
Infarto da Artéria Cerebral Média/prevenção & controle
Fármacos Neuroprotetores/farmacologia
Tretinoína/farmacologia
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Isquemia Encefálica/prevenção & controle
Proteína GAP-43/genética
Imuno-Histoquímica
Infarto da Artéria Cerebral Média/metabolismo
Infarto da Artéria Cerebral Média/patologia
Masculino
Distribuição Aleatória
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
Reprodutibilidade dos Testes
Fatores de Tempo
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GAP-43 Protein); 0 (Neuroprotective Agents); 5688UTC01R (Tretinoin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE


  9 / 2254 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28351388
[Au] Autor:Pan R; Cai J; Zhan L; Guo Y; Huang RY; Li X; Zhou M; Xu D; Zhan J; Chen H
[Ad] Endereço:Department of Rehabilitation, Hospital of Guangzhou Higher Education Mega Center, Guangdong Provincial Hospital of Chinese Medicine, No. 55 Neihuan Xi Road, Guangzhou, Guangdong, 510006, China.
[Ti] Título:Buyang Huanwu decoction facilitates neurorehabilitation through an improvement of synaptic plasticity in cerebral ischemic rats.
[So] Source:BMC Complement Altern Med;17(1):173, 2017 Mar 28.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Loss of neural function is a critical but unsolved issue after cerebral ischemia insult. Neuronal plasticity and remodeling are crucial for recovery of neural functions after brain injury. Buyang Huanwu decoction, which is a classic formula in traditional Chinese medicine, can positively alter synaptic plasticity. This study assessed the effects of Buyang Huanwu decoction in combination with physical exercise on neuronal plasticity in cerebral ischemic rats. METHODS: Cerebral ischemic rats were administered Buyang Huanwu decoction and participated in physical exercise after the induction of a permanent middle cerebral artery occlusion. The neurobehavioral functions and infarct volumes were evaluated. The presynaptic (SYN), postsynaptic (GAP-43) and cytoskeletal (MAP-2) proteins in the coronal brain samples were evaluated by immunohistochemistry and western blot analyses. The ultrastructure of the neuronal synaptic junctions in the same region were analyzed using transmission electron microscopy. RESULTS: Combination treatment of Buyang Huanwu decoction and physical exercise ameliorated the neurobehavioral deficits (p < 0.05), significantly enhanced the expression levels of SYN, GAP-43 and MAP-2 (p < 0.05), and maintained the synaptic ultrastructure. CONCLUSIONS: Buyang Huanwu decoction facilitated neurorehabilitation following a cerebral ischemia insult through an improvement in synaptic plasticity. Graphical abstract The Buyang Huanwu decoction (BYHWD) combined with physical exercise (PE) attenuates synaptic disruption and promotes synaptic plasticity following cerebral ischemia (stroke).
[Mh] Termos MeSH primário: Isquemia Encefálica/tratamento farmacológico
Isquemia Encefálica/reabilitação
Medicamentos de Ervas Chinesas/administração & dosagem
Plasticidade Neuronal/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Isquemia Encefálica/metabolismo
Isquemia Encefálica/fisiopatologia
Proteína GAP-43/genética
Proteína GAP-43/metabolismo
Seres Humanos
Masculino
Proteínas Associadas aos Microtúbulos/genética
Proteínas Associadas aos Microtúbulos/metabolismo
Reabilitação Neurológica
Fármacos Neuroprotetores/administração & dosagem
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drugs, Chinese Herbal); 0 (GAP-43 Protein); 0 (Microtubule-Associated Proteins); 0 (Mtap2 protein, mouse); 0 (Neuroprotective Agents); 0 (buyang huanwu)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170425
[Lr] Data última revisão:
170425
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170330
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1680-9


  10 / 2254 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28339015
[Au] Autor:Huang TQ; Song JN; Zheng FW; Pang HG; Zhao YL; Gu H; Zhao JJ
[Ad] Endereço:Department of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
[Ti] Título:Protection of FK506 against neuronal apoptosis and axonal injury following experimental diffuse axonal injury.
[So] Source:Mol Med Rep;15(5):3001-3010, 2017 May.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Diffuse axonal injury (DAI) is the most common and significant pathological features of traumatic brain injury (TBI). However, there are still no effective drugs to combat the formation and progression of DAI in affected individuals. FK506, also known as tacrolimus, is an immunosuppressive drug, which is widely used in transplantation medicine for the reduction of allograft rejection. Previous studies have identified that FK506 may play an important role in the nerve protective effect of the central nervous system. In the present study, apoptosis of neuronal cells was observed following the induction of experimental DAI. The results demonstrated that it was closely related with the upregulation of death­associated protein kinase 1 (DAPK1). It was hypothesized that FK506 may inhibit the activity of DAPK1 by inhibiting calcineurin activity, which may be primarily involved in anti­apoptosis following DAI induction. Through researching the expression of nerve regeneration associated proteins (NF­H and GAP­43) following DAI, the present study provides novel data to suggest that FK506 promotes axon formation and nerve regeneration following experimental DAI. Therefore, FK506 may be a potent therapeutic for inhibiting nerve injury, as well as promoting the nerve regeneration following DAI.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Axônios/efeitos dos fármacos
Lesão Axonal Difusa/tratamento farmacológico
Tacrolimo/farmacologia
[Mh] Termos MeSH secundário: Animais
Axônios/metabolismo
Axônios/patologia
Lesões Encefálicas Traumáticas/tratamento farmacológico
Lesões Encefálicas Traumáticas/metabolismo
Lesões Encefálicas Traumáticas/patologia
Tronco Encefálico/efeitos dos fármacos
Tronco Encefálico/patologia
Região CA1 Hipocampal/efeitos dos fármacos
Região CA1 Hipocampal/patologia
Calcineurina/efeitos dos fármacos
Proteínas Quinases Associadas com Morte Celular/antagonistas & inibidores
Proteínas Quinases Associadas com Morte Celular/metabolismo
Lesão Axonal Difusa/metabolismo
Lesão Axonal Difusa/patologia
Proteína GAP-43/metabolismo
Masculino
Regeneração Nervosa/efeitos dos fármacos
Proteínas de Neurofilamentos/metabolismo
Ratos
Ratos Sprague-Dawley
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GAP-43 Protein); 0 (Neurofilament Proteins); 108688-71-7 (neurofilament protein H); EC 2.7.11.1 (Death-Associated Protein Kinases); EC 3.1.3.16 (Calcineurin); WM0HAQ4WNM (Tacrolimus)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2017.6350



página 1 de 226 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde