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Pesquisa : D02.691.850.900.950 [Categoria DeCS]
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[PMID]:27729293
[Au] Autor:Sandström J; Eggermann E; Charvet I; Roux A; Toni N; Greggio C; Broyer A; Monnet-Tschudi F; Stoppini L
[Ad] Endereço:Department of Physiology, University of Lausanne, SCAHT, Switzerland.
[Ti] Título:Development and characterization of a human embryonic stem cell-derived 3D neural tissue model for neurotoxicity testing.
[So] Source:Toxicol In Vitro;38:124-135, 2017 Feb.
[Is] ISSN:1879-3177
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Alternative models for more rapid compound safety testing are of increasing demand. With emerging techniques using human pluripotent stem cells, the possibility of generating human in vitro models has gained interest, as factors related to species differences could be potentially eliminated. When studying potential neurotoxic effects of a compound it is of crucial importance to have both neurons and glial cells. We have successfully developed a protocol for generating in vitro 3D human neural tissues, using neural progenitor cells derived from human embryonic stem cells. These 3D neural tissues can be maintained for two months and undergo progressive differentiation. We showed a gradual decreased expression of early neural lineage markers, paralleled by an increase in markers specific for mature neurons, astrocytes and oligodendrocytes. At the end of the two-month culture period the neural tissues not only displayed synapses and immature myelin sheaths around axons, but electrophysiological measurements also showed spontaneous activity. Neurotoxicity testing - comparing non-neurotoxic to known neurotoxic model compounds - showed an expected increase in the marker of astroglial reactivity after exposure to known neurotoxicants methylmercury and trimethyltin. Although further characterization and refinement of the model is required, these results indicate its potential usefulness for in vitro neurotoxicity testing.
[Mh] Termos MeSH primário: Astrócitos/citologia
Células-Tronco Embrionárias Humanas/citologia
Células-Tronco Neurais/citologia
Oligodendroglia/citologia
[Mh] Termos MeSH secundário: Técnicas de Cultura de Células
Diferenciação Celular
Linhagem Celular
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Ibuprofeno/toxicidade
Compostos de Metilmercúrio/toxicidade
Paraquat/toxicidade
RNA Mensageiro/metabolismo
Esferoides Celulares/citologia
Esferoides Celulares/efeitos dos fármacos
Esferoides Celulares/metabolismo
Esferoides Celulares/ultraestrutura
Técnicas de Cultura de Tecidos
Compostos de Trimetilestanho/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Methylmercury Compounds); 0 (RNA, Messenger); 0 (Trimethyltin Compounds); 9E3BCA3684 (trimethyltin chloride); PLG39H7695 (Paraquat); RWZ4L3O1X0 (methylmercuric chloride); WK2XYI10QM (Ibuprofen)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170330
[Lr] Data última revisão:
170330
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161013
[St] Status:MEDLINE


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[PMID]:28263538
[Au] Autor:Stara V; Navarova J; Ujhazy E; Gasparova Z
[Ad] Endereço:Institute of Experimental Pharmacology and Toxicology, SAS, Slovakia.
[Ti] Título:Progressive increase of lysosomal enzyme activities in hippocampus associated with reduction of population spike in a rat model of neurodegeneration.
[So] Source:Neuro Endocrinol Lett;37(Suppl1):111-117, 2016 Dec 18.
[Is] ISSN:0172-780X
[Cp] País de publicação:Sweden
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Extensive effort has been made to identify early markers of neurodegeneration as late stages have no chance of treatment. Recently, many experimental models have been used to study hallmarks of neuronal injury. One of them is the model of trimethyltin (TMT)-induced damage associated with cognitive decline, thus called a model of Alzheimer-like disease. OBJECTIVE AND METHODS: Our aim was to study neuronal transmission in hippocampal slices of male Wistar rats affected with a single dose of TMT (7.5 mg/kg, i.p.) during the first three weeks of its action. The monitored time periods after TMT administration were days 1-3; 8-10 and 15-17. At the same time periods, right hippocampi were collected for determination of changes in specific activities of two lysosomal enzymes. Electrophysiological measurements were based on stimulation of Schäffer collaterals and registration of evoked responses in the stratum pyramidale and the stratum radiatum at the CA3-CA1 synapse. Specific activities of N-acetyl-ß-D-glucosaminidase (NAGA) and cathepsin D (Cat D) were determined spectrophotometrically. RESULTS: During three weeks after i.p. TMT administration to rats, we found a time-dependent reduction of postsynaptic neuronal firing, expressed by diminished population spike (PoS) amplitude recorded in the stratum pyramidale accompanied with marked increase in specific activity of NAGA to respective 111%, 163% and 252% in the 1st, 2nd and 3rd week compared to unaffected rats. In the stratum radiatum, reduction of the slope of excitatory postsynaptic potential was not time-dependent but almost constantly reduced from the 1st to 3rd week after TMT administration (55-60%) compared to control rats. Specific activity of lysosomal enzyme Cat D was significantly increased in the 3rd week after TMT administration. CONCLUSION: This work demonstrates a time-dependent reduction of somatic response in the hippocampus of TMT affected rats during the first three weeks. This reduction of neuronal firing was later accompanied with increase of specific activity of NAGA and Cat D, supporting evidence that lysosomal dysfunction may be one of the primary contributors to TMT-induced neurodegeneration.
[Mh] Termos MeSH primário: Hipocampo/enzimologia
Lisossomos/enzimologia
Doenças Neurodegenerativas/enzimologia
Compostos de Trimetilestanho/farmacologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Potenciais Evocados
Hipocampo/efeitos dos fármacos
Hipocampo/fisiopatologia
Lisossomos/efeitos dos fármacos
Masculino
Doenças Neurodegenerativas/induzido quimicamente
Doenças Neurodegenerativas/fisiopatologia
Neurônios/fisiologia
Ratos
Ratos Wistar
Compostos de Trimetilestanho/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Trimethyltin Compounds); 1631-73-8 (trimethyltin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170307
[St] Status:MEDLINE


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[PMID]:28105250
[Au] Autor:Kang JY; Park SK; Guo TJ; Ha JS; Lee DS; Kim JM; Lee U; Kim DO; Heo HJ
[Ad] Endereço:Division of Applied Life Science (BK21 Plus), Institute of Agriculture and Life Science, Gyeongsang National University, Jinju 52828, Republic of Korea.
[Ti] Título:Reversal of Trimethyltin-Induced Learning and Memory Deficits by 3,5-Dicaffeoylquinic Acid.
[So] Source:Oxid Med Cell Longev;2016:6981595, 2016.
[Is] ISSN:1942-0994
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The antiamnesic effect of 3,5-dicaffeoylquinic acid (3,5-diCQA) as the main phenolic compound in H. extract on cognitive dysfunction induced by trimethyltin (TMT) (7.1 g/kg of body weight; intraperitoneal injection) was investigated in order to assess its ameliorating function in mice. In several behavioral tests, namely, the Y-maze, passive avoidance, and Morris water maze (MWM) test, 3,5-diCQA significantly ameliorated learning and memory deficits. After the behavioral tests, brain tissues from the mice were analyzed to characterize the basis of the neuroprotective effect. Acetylcholine (ACh) levels increased, whereas the activity of acetylcholinesterase (AChE) decreased upon administration of 3,5-diCQA. In addition, 3,5-diCQA effectively protected against an increase in malondialdehyde (MDA) content, an increase in the oxidized glutathione (GSH) ratio, and a decline of total superoxide dismutase (SOD) level. 3,5-diCQA may prevent neuronal apoptosis through the protection of mitochondrial activities and the repression of apoptotic signaling molecules such as p-Akt, BAX, and p-tau (Ser 404).
[Mh] Termos MeSH primário: Ácido Clorogênico/análogos & derivados
Aprendizagem em Labirinto/efeitos dos fármacos
Memória/efeitos dos fármacos
Fármacos Neuroprotetores/uso terapêutico
Compostos de Trimetilestanho/toxicidade
[Mh] Termos MeSH secundário: Acetilcolinesterase/metabolismo
Animais
Artemisia/química
Artemisia/metabolismo
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Ácido Clorogênico/química
Ácido Clorogênico/farmacologia
Ácido Clorogênico/uso terapêutico
Cromatografia Líquida de Alta Pressão
Glutationa/metabolismo
Glicogênio Sintase Quinase 3 beta/metabolismo
Malondialdeído/metabolismo
Transtornos da Memória/tratamento farmacológico
Camundongos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Fármacos Neuroprotetores/farmacologia
Extratos Vegetais/análise
Extratos Vegetais/química
Extratos Vegetais/farmacologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Superóxido Dismutase/metabolismo
Espectrometria de Massas em Tandem
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuroprotective Agents); 0 (Plant Extracts); 0 (Trimethyltin Compounds); 0 (bcl-2-Associated X Protein); 1631-73-8 (trimethyltin); 318ADP12RI (Chlorogenic Acid); 4Y8F71G49Q (Malondialdehyde); EC 1.15.1.1 (Superoxide Dismutase); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.1.1.7 (Acetylcholinesterase); GAN16C9B8O (Glutathione); ND94C5E75K (3,5-dicaffeoylquinic acid)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170121
[St] Status:MEDLINE
[do] DOI:10.1155/2016/6981595


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[PMID]:27614947
[Au] Autor:Lee S; Kang S; Kim J; Yoon S; Kim SH; Moon C
[Ad] Endereço:Department of Veterinary Anatomy, College of Veterinary Medicine and BK21 Plus Project Team, Animal Medical Institute, Chonnam National University, Gwangju 61186, South Korea.
[Ti] Título:Enhanced expression of immediate-early genes in mouse hippocampus after trimethyltin treatment.
[So] Source:Acta Histochem;118(7):679-684, 2016 Sep.
[Is] ISSN:1618-0372
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Immediate-early genes (IEGs) are transiently and rapidly activated in response to various cellular stimuli. IEGs mediate diverse functions during pathophysiologic events by regulating cellular signal transduction. We investigated the temporal expression of several IEGs, including c-fos, early growth response protein-1 (Egr-1), and activity-regulated cytoskeleton-associated protein (Arc), in trimethyltin (TMT)-induced hippocampal neurodegeneration. Mice (7 weeks old, C57BL/6) administered TMT (2.6mg/kg intraperitoneally) presented severe neurodegenerative lesions in the dentate gyrus (DG) and showed behavioral seizure activity on days 1-4 post-treatment, after which the lesions and behavior recovered spontaneously over time. c-fos, Egr-1, and Arc mRNA and protein levels significantly increased in the mouse hippocampus after TMT treatment. Immunohistochemical analysis showed that nuclear c-fos expression increased mainly in the DG, whereas nuclear Egr-1 expression was increased extensively in cornu ammonis (CA) 1, CA3, and the DG after TMT treatment. Increased Arc levels were detected in the cellular somata/dendrites of the hippocampal subregions after TMT treatment. Therefore, we suggest that increased IEGs are associated with TMT-induced pathological events in mouse hippocampus.
[Mh] Termos MeSH primário: Giro Denteado/efeitos dos fármacos
Genes Precoces/efeitos dos fármacos
Hipocampo/efeitos dos fármacos
Hipocampo/metabolismo
Neurônios/efeitos dos fármacos
Compostos de Trimetilestanho/farmacologia
[Mh] Termos MeSH secundário: Animais
Giro Denteado/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Proteínas do Tecido Nervoso/metabolismo
Neurônios/metabolismo
Proteínas Proto-Oncogênicas c-fos/metabolismo
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nerve Tissue Proteins); 0 (Proto-Oncogene Proteins c-fos); 0 (RNA, Messenger); 0 (Trimethyltin Compounds); 1631-73-8 (trimethyltin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170227
[Lr] Data última revisão:
170227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160912
[St] Status:MEDLINE


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[PMID]:27450702
[Au] Autor:Lee S; Yang M; Kim J; Kang S; Kim J; Kim JC; Jung C; Shin T; Kim SH; Moon C
[Ad] Endereço:Departments of Veterinary Anatomy and Veterinary Toxicology, College of Veterinary Medicine and BK21 Plus Project Team, Chonnam National University, Gwangju 61186, South Korea.
[Ti] Título:Trimethyltin-induced hippocampal neurodegeneration: A mechanism-based review.
[So] Source:Brain Res Bull;125:187-99, 2016 Jul.
[Is] ISSN:1873-2747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Trimethyltin (TMT), a toxic organotin compound, induces neurodegeneration selectively involving the limbic system and especially prominent in the hippocampus. Neurodegeneration-associated behavioral abnormalities, such as hyperactivity, aggression, cognitive deficits, and epileptic seizures, occur in both exposed humans and experimental animal models. Previously, TMT had been used generally in industry and agriculture, but the use of TMT has been limited because of its dangers to people. TMT has also been used to make a promising in vivo rodent model of neurodegeneration because of its region-specific characteristics. Several studies have demonstrated that TMT-treated animal models of epileptic seizures can be used as tools for researching hippocampus-specific neurotoxicity as well as the molecular mechanisms leading to hippocampal neurodegeneration. This review summarizes the in vivo and in vitro underlying mechanisms of TMT-induced hippocampal neurodegeneration (oxidative stress, inflammatory responses, and neuronal death/survival). Thus, the present review may be helpful to provide general insights into TMT-induced neurodegeneration and approaches to therapeutic interventions for neurodegenerative diseases, including temporal lobe epilepsy.
[Mh] Termos MeSH primário: Hipocampo/efeitos dos fármacos
Degeneração Neural/induzido quimicamente
Compostos Orgânicos de Estanho/toxicidade
Compostos de Trimetilestanho/toxicidade
[Mh] Termos MeSH secundário: Animais
Morte Celular/efeitos dos fármacos
Inflamação/induzido quimicamente
Estresse Oxidativo/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Organotin Compounds); 0 (Trimethyltin Compounds); 1631-73-8 (trimethyltin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160725
[St] Status:MEDLINE


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[PMID]:27374288
[Au] Autor:Kim CR; Choi SJ; Kwon YK; Kim JK; Kim YJ; Park GG; Shin DH
[Ad] Endereço:Department of Food and Biotechnology, Korea University.
[Ti] Título:Cinnamomum loureirii Extract Inhibits Acetylcholinesterase Activity and Ameliorates Trimethyltin-Induced Cognitive Dysfunction in Mice.
[So] Source:Biol Pharm Bull;39(7):1130-6, 2016.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The pathogenesis of Alzheimer's disease (AD) has been linked to the deficiency of neurotransmitter acetylcholine (ACh) in the brain, and the main treatment strategy for improving AD symptoms is the inhibition of acetylcholinesterase (AChE) activity. In the present study, we aimed to identify potent AChE inhibitors from Cinnamomum loureirii extract via bioassay-guided fractionation. We demonstrated that the most potent AChE inhibitor present in the C. loureirii extract was 2,4-bis(1,1-dimethylethyl)phenol. To confirm the antiamnesic effects of the ethanol extract of C. loureirii, mice were intraperitoneally injected with the neurotoxin trimethyltin (2.5 mg/kg) to induce cognitive dysfunction, and performance in the Y-maze and passive avoidance tests was assessed. Treatment with C. loureirii extract significantly improved performance in both behavioral tests, suggesting that this extract may be neuroprotective and therefore beneficial in preventing or ameliorating the degenerative processes of AD, potentially by restoring cholinergic function.
[Mh] Termos MeSH primário: Inibidores da Colinesterase/farmacologia
Inibidores da Colinesterase/uso terapêutico
Cinnamomum
Disfunção Cognitiva/tratamento farmacológico
Extratos Vegetais/farmacologia
Extratos Vegetais/uso terapêutico
[Mh] Termos MeSH secundário: Acetilcolinesterase/metabolismo
Animais
Aprendizagem da Esquiva/efeitos dos fármacos
Comportamento Animal/efeitos dos fármacos
Linhagem Celular Tumoral
Inibidores da Colinesterase/isolamento & purificação
Disfunção Cognitiva/induzido quimicamente
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Camundongos Endogâmicos ICR
Neurotoxinas
Fenóis/isolamento & purificação
Fenóis/farmacologia
Fenóis/uso terapêutico
Fitoterapia
Extratos Vegetais/química
Ratos
Compostos de Trimetilestanho
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholinesterase Inhibitors); 0 (Neurotoxins); 0 (Phenols); 0 (Plant Extracts); 0 (Trimethyltin Compounds); 1631-73-8 (trimethyltin); EC 3.1.1.7 (Acetylcholinesterase)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170127
[Lr] Data última revisão:
170127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160705
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00045


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[PMID]:27167774
[Au] Autor:Mengeling BJ; Murk AJ; Furlow JD
[Ad] Endereço:Department of Neurobiology, Physiology and Behavior (B.J.M., J.D.F.), University of California Davis, Davis, California 95695; and Marine Animal Ecology Group (A.J.M.), Wageningen University, 6700 AH Wageningen, The Netherlands.
[Ti] Título:Trialkyltin Rexinoid-X Receptor Agonists Selectively Potentiate Thyroid Hormone Induced Programs of Xenopus laevis Metamorphosis.
[So] Source:Endocrinology;157(7):2712-23, 2016 Jul.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The trialkyltins tributyltin (TBT) and triphenyltin (TPT) can function as rexinoid-X receptor (RXR) agonists. We recently showed that RXR agonists can alter thyroid hormone (TH) signaling in a mammalian pituitary TH-responsive reporter cell line, GH3.TRE-Luc. The prevalence of TBT and TPT in the environment prompted us to test whether they could also affect TH signaling. Both trialkyltins induced the integrated luciferase reporter alone and potentiated TH activation at low doses. Trimethyltin, which is not an RXR agonist, did not. We turned to a simple, robust, and specific in vivo model system of TH action: metamorphosis of Xenopus laevis, the African clawed frog. Using a precocious metamorphosis assay, we found that 1nM TBT and TPT, but not trimethyltin, greatly potentiated the effect of TH treatment on resorption phenotypes of the tail, which is lost at metamorphosis, and in the head, which undergoes extensive remodeling including gill loss. Consistent with these responses, TH-induced caspase-3 activation in the tail was enhanced by cotreatment with TBT. Induction of a transgenic reporter gene and endogenous collagenase 3 (mmp13) and fibroblast-activating protein-α (fap) genes were not induced by TBT alone, but TH induction was significantly potentiated by TBT. However, induction of other TH receptor target genes such as TRß and deiodinase 3 by TH were not affected by TBT cotreatment. These data indicate that trialkyltins that can function as RXR agonists can selectively potentiate gene expression and resultant morphological programs directed by TH signaling in vivo.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Metamorfose Biológica/efeitos dos fármacos
Receptores X Retinoide/agonistas
Transaminases/farmacologia
Compostos de Trialquitina/farmacologia
[Mh] Termos MeSH secundário: Animais
Caspase 3/metabolismo
Metaloproteinase 13 da Matriz/metabolismo
Compostos Orgânicos de Estanho/farmacologia
Compostos de Trimetilestanho/farmacologia
Xenopus laevis/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Organotin Compounds); 0 (Retinoid X Receptors); 0 (Trialkyltin Compounds); 0 (Trimethyltin Compounds); 1631-73-8 (trimethyltin); 4XDX163P3D (tributyltin); 95T92AGN0V (triphenyltin); EC 2.6.1.- (Transaminases); EC 2.6.1.26 (thyroid hormone aminotransferase); EC 3.4.22.- (Caspase 3); EC 3.4.24.- (Matrix Metalloproteinase 13)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160512
[St] Status:MEDLINE
[do] DOI:10.1210/en.2016-1062


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[PMID]:27143997
[Au] Autor:Zhao W; Pan X; Li T; Zhang C; Shi N
[Ad] Endereço:Department of Health Toxicology, MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
[Ti] Título:Lycium barbarum Polysaccharides Protect against Trimethyltin Chloride-Induced Apoptosis via Sonic Hedgehog and PI3K/Akt Signaling Pathways in Mouse Neuro-2a Cells.
[So] Source:Oxid Med Cell Longev;2016:9826726, 2016.
[Is] ISSN:1942-0994
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Trimethyltin chloride (TMT) is a classic neurotoxicant that can cause severe neurodegenerative diseases. Some signaling pathways involving cell death play pivotal roles in the central nervous system. In this study, the role of Sonic Hedgehog (Shh) and PI3K/Akt pathways in TMT-induced apoptosis and protective effect of Lycium barbarum polysaccharides (LBP) on mouse neuro-2a (N2a) cells were investigated. Results showed that TMT treatment significantly enhanced apoptosis, upregulated proapoptotic Bax, downregulated antiapoptotic Bcl-2 expression, and increased caspase-3 activity in a dose-dependent manner in N2a cells. TMT induced oxidative stress in cells, performing reactive oxygen species (ROS) and malondialdehyde (MDA) excessive generation, and superoxide dismutase (SOD) activity reduction. TMT significantly decreased phosphorylated glycogen synthase kinase-3ß (GSK-3ß) and inhibited Shh and PI3K/Akt pathways. However, the addition of LBP upregulated GSK-3ß phosphorylation, activated Shh and PI3K/Akt pathways, and eventually reduced apoptosis and oxidative stress caused by TMT. The interaction between Shh and PI3K/Akt pathways was clarified by specific PI3K inhibitor LY294002 or Shh inhibitor GDC-0449. Moreover, LY294002 and GDC-0449 pretreatment both induced phosphorylated GSK-3ß downregulation and significantly promoted apoptosis induced by TMT. These results suggest that LBP could reduce TMT-induced N2a cells apoptosis by regulating GSK-3ß phosphorylation, Shh, and PI3K/Akt signaling pathways.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Medicamentos de Ervas Chinesas/farmacologia
Transdução de Sinais/efeitos dos fármacos
Compostos de Trimetilestanho/toxicidade
[Mh] Termos MeSH secundário: Anilidas/farmacologia
Animais
Caspase 3/metabolismo
Linhagem Celular
Cromonas/farmacologia
Glicogênio Sintase Quinase 3 beta/metabolismo
Proteínas Hedgehog/antagonistas & inibidores
Proteínas Hedgehog/metabolismo
Peroxidação de Lipídeos/efeitos dos fármacos
Camundongos
Microscopia de Fluorescência
Morfolinas/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Fosfatidilinositol 3-Quinases/metabolismo
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Piridinas/farmacologia
Espécies Reativas de Oxigênio/metabolismo
Superóxido Dismutase/análise
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anilides); 0 (Chromones); 0 (Drugs, Chinese Herbal); 0 (Hedgehog Proteins); 0 (HhAntag691); 0 (Morpholines); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Pyridines); 0 (Reactive Oxygen Species); 0 (Trimethyltin Compounds); 0 (bcl-2-Associated X Protein); 0 (lycium barbarum polysaccharide); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); 9E3BCA3684 (trimethyltin chloride); EC 1.15.1.1 (Superoxide Dismutase); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170308
[Lr] Data última revisão:
170308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160505
[St] Status:MEDLINE
[do] DOI:10.1155/2016/9826726


  9 / 541 MEDLINE  
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[PMID]:27008919
[Au] Autor:Duan R; Cui Y; Zhao Y; Li C; Chen L; Hou J; Wagner M; Baumgarten M; He C; Müllen K
[Ad] Endereço:Max Planck Institute for Polymer Research, Ackermannweg 10, 55128, Mainz, Germany.
[Ti] Título:The Importance of End Groups for Solution-Processed Small-Molecule Bulk-Heterojunction Photovoltaic Cells.
[So] Source:ChemSusChem;9(9):973-80, 2016 05 10.
[Is] ISSN:1864-564X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:End groups in small-molecule photovoltaic materials are important owing to their strong influence on molecular stability, solubility, energy levels, and aggregation behaviors. In this work, a series of donor-acceptor pentads (D2 -A-D1 -A-D2 ) were designed and synthesized, aiming to investigate the effect of the end groups on the materials properties and photovoltaic device performance. These molecules share identical central A-D1 -A triads (with benzodithiophene as D1 and 6-carbonyl-thieno[3,4-b]thiophene as A), but with various D2 end groups composed of alkyl-substituted thiophene (T), thieno[3,2-b]thiophene (TT), and 2,2'-bithiophene (BT). The results indicate a relationship between conjugated segment/alkyl chain length of the end groups and the photovoltaic performance, which contributes to the evolving molecular design principles for high efficiency organic solar cells.
[Mh] Termos MeSH primário: Fontes de Energia Elétrica
Energia Solar
[Mh] Termos MeSH secundário: Soluções
Tiofenos/química
Compostos de Trimetilestanho/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Solutions); 0 (Thiophenes); 0 (Trimethyltin Compounds)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170316
[Lr] Data última revisão:
170316
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160325
[St] Status:MEDLINE
[do] DOI:10.1002/cssc.201501626


  10 / 541 MEDLINE  
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[PMID]:26915108
[Au] Autor:Toesca A; Geloso MC; Mongiovì AM; Furno A; Schiattarella A; Michetti F; Corvino V
[Ad] Endereço:Institute of Anatomy and Cell Biology, Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 000168, Rome, Italy.
[Ti] Título:Trimethyltin Modulates Reelin Expression and Endogenous Neurogenesis in the Hippocampus of Developing Rats.
[So] Source:Neurochem Res;41(7):1559-69, 2016 Jul.
[Is] ISSN:1573-6903
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Reelin is an extracellular matrix glycoprotein involved in the modulation of synaptic plasticity and essential for the proper radial migration of cortical neurons during development and for the integration and positioning of dentate granular cell progenitors; its expression is down-regulated as brain maturation is completed. Trimethyltin (TMT) is a potent neurotoxicant which causes selective neuronal death mainly localised in the CA1-CA3/hilus hippocampal regions. In the present study we analysed the expression of reelin and the modulation of endogenous neurogenesis in the postnatal rat hippocampus during TMT-induced neurodegeneration (TMT 6 mg/kg). Our results show that TMT administration induces changes in the physiological postnatal decrease of reelin expression in the hippocampus of developing rats. In particular, quantitative analysis of reelin-positive cells evidenced, in TMT-treated animals, a persistent reelin expression in the stratum lacunosum moleculare of Cornu Ammonis and in the molecular layer of Dentate Gyrus. In addition, a significant decrease in the number of bromodeoxyuridine (BrdU)-labeled newly-generated cells was also detectable in the subgranular zone of P21 TMT-treated rats compared with P21 control animals; no differences between P28 TMT-treated rats and age-matched control group were observed. In addition the neuronal commitment of BrdU-positive cells appeared reduced in P21 TMT-treated rats compared with P28 TMT-treated animals. Thus TMT treatment, administrated during development, induces an early reduction of endogenous neurogenesis and influences the hippocampal pattern of reelin expression in a temporally and regionally specific manner, altering the physiological decrease of this protein.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular Neuronais/biossíntese
Proteínas da Matriz Extracelular/biossíntese
Regulação da Expressão Gênica no Desenvolvimento
Hipocampo/crescimento & desenvolvimento
Hipocampo/metabolismo
Proteínas do Tecido Nervoso/biossíntese
Neurogênese/fisiologia
Serina Endopeptidases/biossíntese
Compostos de Trimetilestanho/farmacologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Moléculas de Adesão Celular Neuronais/antagonistas & inibidores
Moléculas de Adesão Celular Neuronais/genética
Proteínas da Matriz Extracelular/antagonistas & inibidores
Proteínas da Matriz Extracelular/genética
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Hipocampo/efeitos dos fármacos
Proteínas do Tecido Nervoso/antagonistas & inibidores
Proteínas do Tecido Nervoso/genética
Neurogênese/efeitos dos fármacos
Plasticidade Neuronal/efeitos dos fármacos
Plasticidade Neuronal/fisiologia
Ratos
Ratos Wistar
Serina Endopeptidases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Adhesion Molecules, Neuronal); 0 (Extracellular Matrix Proteins); 0 (Nerve Tissue Proteins); 0 (Trimethyltin Compounds); 1631-73-8 (trimethyltin); EC 3.4.21.- (Serine Endopeptidases); EC 3.4.21.- (reelin protein)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160226
[St] Status:MEDLINE
[do] DOI:10.1007/s11064-016-1869-1



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