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Pesquisa : D03.383.773.165 [Categoria DeCS]
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[PMID]:28480948
[Au] Autor:Yildirim A; Lübbers HT; Yildirim A
[Ad] Endereço:Clinique de soins intensifs chirurgicaux, Hôpital universitaire de Zurich, Zurich, Switzerland.
[Ti] Título:Anaphylaxie induite par des médicaments..
[So] Source:Swiss Dent J;127(4):324-325, 2017.
[Is] ISSN:2296-6498
[Cp] País de publicação:Switzerland
[La] Idioma:fre
[Ab] Resumo:Anaphylaxis is defined as a serious allergic or hypersensitivity reaction in the most cases as a result of an IgE-mediated allergic reaction that is rapid in onset and may cause death. Common triggers are foods, insect stings, and medications. The medical treatment includes, epinephrine, glucocorticoids, antihistamines and inhaled bronchodilators, with the aim to prevent progression to life-threatening respiratory and/or cardiovascular symptoms.
[Mh] Termos MeSH primário: Anafilaxia/induzido quimicamente
Anafilaxia/tratamento farmacológico
Clemastina/uso terapêutico
Epinefrina/uso terapêutico
Antagonistas dos Receptores Histamínicos/uso terapêutico
Hemissuccinato de Metilprednisolona/uso terapêutico
Ressuscitação
[Mh] Termos MeSH secundário: Terapia Combinada
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histamine Antagonists); 5GMR90S4KN (Methylprednisolone Hemisuccinate); 95QN29S1ID (Clemastine); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE


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[PMID]:27865736
[Au] Autor:Nicaise AM; Banda E; Guzzo RM; Russomanno K; Castro-Borrero W; Willis CM; Johnson KM; Lo AC; Crocker SJ
[Ad] Endereço:Department of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Ave., Farmington, CT 06032, United States.
[Ti] Título:iPS-derived neural progenitor cells from PPMS patients reveal defect in myelin injury response.
[So] Source:Exp Neurol;288:114-121, 2017 Feb.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Primary progressive multiple sclerosis (PPMS) is a chronic demyelinating disease of the central nervous system (CNS) currently lacking any effective treatment. Promoting endogenous brain repair offers a potential strategy to halt and possibly restore neurologic function in PPMS. To understand how the microenvironment within white matter lesions plays a role in repair we have focused on neural progenitor cells (NPCs) since these are found in lesions in PPMS and have been found to influence oligodendrocyte progenitor cell maturation (OPCs). To better understand the cellular nature of NPCs in PPMS we developed iPS cells from blood samples of PPMS patients and age matched non-disease spouse or blood relative controls. Using these iPS cell lines we determined that the NPCs from PPMS cases provided no neuroprotection against active CNS demyelination compared to NPCs from control iPS lines which were capable of completely preventing injury. Conditioned media (CM) from PPMS NPCs provides no protection to OPCs and prevents maturation of OPCs into oligodendrocytes in vitro. We also found that CM from PPMS iPS NPCs elicited patient-specific differences in the response to compounds that should foster oligodendrocyte (OL) maturation. Together, these data establish a new model for understanding the nature of myelination defects in PPMS which may lead to novel targeted approaches for preventing demyelination in these patients.
[Mh] Termos MeSH primário: Células-Tronco Pluripotentes Induzidas/patologia
Esclerose Múltipla Crônica Progressiva/patologia
Bainha de Mielina/patologia
[Mh] Termos MeSH secundário: Idoso
Animais
Apoptose/efeitos dos fármacos
Axônios/patologia
Axônios/ultraestrutura
Diferenciação Celular/efeitos dos fármacos
Clemastina/farmacologia
Clemastina/uso terapêutico
Meios de Cultivo Condicionados/farmacologia
Cuprizona/toxicidade
Feminino
Seres Humanos
Células-Tronco Pluripotentes Induzidas/química
Células-Tronco Pluripotentes Induzidas/efeitos dos fármacos
Células-Tronco Pluripotentes Induzidas/ultraestrutura
Masculino
Camundongos Endogâmicos C57BL
Miconazol/farmacologia
Miconazol/uso terapêutico
Meia-Idade
Inibidores da Monoaminoxidase/toxicidade
Esclerose Múltipla Crônica Progressiva/induzido quimicamente
Proteína Básica da Mielina/metabolismo
Bainha de Mielina/ultraestrutura
Proteínas do Tecido Nervoso/metabolismo
Oligodendroglia/efeitos dos fármacos
Oligodendroglia/patologia
Oligodendroglia/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media, Conditioned); 0 (Mbp protein, mouse); 0 (Monoamine Oxidase Inhibitors); 0 (Myelin Basic Protein); 0 (Nerve Tissue Proteins); 5N16U7E0AO (Cuprizone); 7NNO0D7S5M (Miconazole); 95QN29S1ID (Clemastine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170512
[Lr] Data última revisão:
170512
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161121
[St] Status:MEDLINE


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[PMID]:27549088
[Au] Autor:Apolloni S; Fabbrizio P; Amadio S; Volonté C
[Ad] Endereço:Santa Lucia Foundation, IRCCS, Rome, Italy.
[Ti] Título:Actions of the antihistaminergic clemastine on presymptomatic SOD1-G93A mice ameliorate ALS disease progression.
[So] Source:J Neuroinflammation;13(1):191, 2016 Aug 22.
[Is] ISSN:1742-2094
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a disease with a strong neuroinflammatory component sustained by activated microglia contributing to motoneuron death. However, how to successfully balance neuroprotective versus neurotoxic actions by the use of antinflammatory agents is still under scrutiny. We have recently shown that the antihistamine clemastine, an FDA-approved drug, can influence the M1/M2 switch occurring in SOD1-G93A ALS microglia. METHODS: Here, we have chronically treated female SOD1-G93A mice with clemastine, evaluated disease progression and performed mice lumbar spinal cord analysis at symptomatic and end stage of the disease. Moreover, we have studied the mechanism of action of clemastine in primary adult spinal SOD1-G93A microglia cultures and in NSC-G93A motor neuron-like cells. RESULTS: We found that a short treatment with clemastine (50 mg/kg) from asymptomatic (postnatal day 40) to symptomatic phase (postnatal day 120) significantly delayed disease onset and extended the survival of SOD1-G93A mice by about 10 %. Under these conditions, clemastine induced protection of motor neurons, modulation of inflammatory parameters, reduction of SOD1 protein levels and SQSTM1/p62 autophagic marker, when analysed immediately at the end of the treatment (postnatal day 120). A long treatment with clemastine (from asymptomatic until the end stage) instead failed to ameliorate ALS disease progression. At the end stage of the disease, we found that clemastine short treatment decreased microgliosis and SOD1 protein and increased LC3-II autophagic marker, while the long treatment produced opposite effects. Finally, in spinal microglia cultures from symptomatic SOD1-G93A mice clemastine activated inflammatory parameters, stimulated autophagic flux via the mTOR signalling pathway and decreased SOD1 levels. Modulation of autophagy was also demonstrated in NSC34 SOD1-G93A motor neuron-like cells. CONCLUSIONS: By gaining insights into the ameliorating actions of an antihistaminergic compound in ALS disease, our findings might represent an exploitable therapeutic approach for familial forms of ALS.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/genética
Esclerose Amiotrófica Lateral/prevenção & controle
Clemastina/uso terapêutico
Antagonistas dos Receptores Histamínicos/uso terapêutico
Superóxido Dismutase/genética
[Mh] Termos MeSH secundário: Esclerose Amiotrófica Lateral/patologia
Animais
Animais Recém-Nascidos
Doenças Assintomáticas/terapia
Autofagia/efeitos dos fármacos
Células Cultivadas
Citocinas/metabolismo
Modelos Animais de Doenças
Progressão da Doença
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Microglia/efeitos dos fármacos
Neurônios Motores/efeitos dos fármacos
Neurônios Motores/patologia
Receptores Purinérgicos P2X4/metabolismo
Transdução de Sinais/efeitos dos fármacos
Medula Espinal/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Histamine Antagonists); 0 (Receptors, Purinergic P2X4); 95QN29S1ID (Clemastine); EC 1.15.1.1 (SOD1 G93A protein); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160824
[St] Status:MEDLINE
[do] DOI:10.1186/s12974-016-0658-8


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[PMID]:27082760
[Au] Autor:De Rycker M; Thomas J; Riley J; Brough SJ; Miles TJ; Gray DW
[Ad] Endereço:Drug Discovery Unit, Division of Biological Chemistry and Drug Discovery, University of Dundee, Dundee, United Kingdom.
[Ti] Título:Identification of Trypanocidal Activity for Known Clinical Compounds Using a New Trypanosoma cruzi Hit-Discovery Screening Cascade.
[So] Source:PLoS Negl Trop Dis;10(4):e0004584, 2016 Apr.
[Is] ISSN:1935-2735
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chagas disease is a significant health problem in Latin America and the available treatments have significant issues in terms of toxicity and efficacy. There is thus an urgent need to develop new treatments either via a repurposing strategy or through the development of new chemical entities. A key first step is the identification of compounds with anti-Trypanosoma cruzi activity from compound libraries. Here we describe a hit discovery screening cascade designed to specifically identify hits that have the appropriate anti-parasitic properties to warrant further development. The cascade consists of a primary imaging-based assay followed by newly developed and appropriately scaled secondary assays to predict the cidality and rate-of-kill of the compounds. Finally, we incorporated a cytochrome P450 CYP51 biochemical assay to remove compounds that owe their phenotypic response to inhibition of this enzyme. We report the use of the cascade in profiling two small libraries containing clinically tested compounds and identify Clemastine, Azelastine, Ifenprodil, Ziprasidone and Clofibrate as molecules having appropriate profiles. Analysis of clinical derived pharmacokinetic and toxicity data indicates that none of these are appropriate for repurposing but they may represent suitable start points for further optimisation for the treatment of Chagas disease.
[Mh] Termos MeSH primário: Avaliação Pré-Clínica de Medicamentos
Tripanossomicidas/isolamento & purificação
Tripanossomicidas/farmacologia
Trypanosoma cruzi/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antipiréticos/farmacologia
Linhagem Celular
Cercopithecus aethiops
Doença de Chagas/tratamento farmacológico
Doença de Chagas/parasitologia
Clemastina/farmacologia
Reposicionamento de Medicamentos
Ensaios de Triagem em Larga Escala
Testes de Sensibilidade Parasitária
Esterol 14-Desmetilase
Tripanossomicidas/química
Trypanosoma cruzi/crescimento & desenvolvimento
Trypanosoma cruzi/ultraestrutura
Células Vero
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antipyretics); 0 (Trypanocidal Agents); 95QN29S1ID (Clemastine); EC 1.14.13.70 (Sterol 14-Demethylase)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160416
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pntd.0004584


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[PMID]:26791223
[Au] Autor:Liu J; Dupree JL; Gacias M; Frawley R; Sikder T; Naik P; Casaccia P
[Ad] Endereço:Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029, and Jia.Liu@mssm.edu.
[Ti] Título:Clemastine Enhances Myelination in the Prefrontal Cortex and Rescues Behavioral Changes in Socially Isolated Mice.
[So] Source:J Neurosci;36(3):957-62, 2016 Jan 20.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Altered myelin structure and oligodendrocyte function have been shown to correlate with cognitive and motor dysfunction and deficits in social behavior. We and others have previously demonstrated that social isolation in mice induced behavioral, transcriptional, and ultrastructural changes in oligodendrocytes of the prefrontal cortex (PFC). However, whether enhancing myelination and oligodendrocyte differentiation could be beneficial in reversing such changes remains unexplored. To test this hypothesis, we orally administered clemastine, an antimuscarinic compound that has been shown to enhance oligodendrocyte differentiation and myelination in vitro, for 2 weeks in adult mice following social isolation. Clemastine successfully reversed social avoidance behavior in mice undergoing prolonged social isolation. Impaired myelination was rescued by oral clemastine treatment, and was associated with enhanced oligodendrocyte progenitor differentiation and epigenetic changes. Clemastine induced higher levels of repressive histone methylation (H3K9me3), a marker for heterochromatin, in oligodendrocytes, but not neurons, of the PFC. This was consistent with the capability of clemastine in elevating H3K9 histone methyltransferases activity in cultured primary mouse oligodendrocytes, an effect that could be antagonized by cotreatment with muscarine. Our data suggest that promoting adult myelination is a potential strategy for reversing depressive-like social behavior. Significance statement: Oligodendrocyte development and myelination are highly dynamic processes influenced by experience and neuronal activity. However, whether enhancing myelination and oligodendrocyte differentiation is beneficial to treat depressive-like behavior has been unexplored. Mice undergoing prolonged social isolation display impaired myelination in the prefrontal cortex. Clemastine, a Food and Drug Administration-approved antimuscarinic compound that has been shown to enhance myelination under demyelinating conditions, successfully reversed social avoidance behavior in adult socially isolated mice. This was associated with enhanced myelination and oligodendrocyte differentiation in the prefrontal cortex through epigenetic regulation. Thus, enhancing myelination may be a potential means of reversing depressive-like social behavior.
[Mh] Termos MeSH primário: Aprendizagem da Esquiva/fisiologia
Clemastina/farmacologia
Bainha de Mielina/metabolismo
Fibras Nervosas Mielinizadas/metabolismo
Córtex Pré-Frontal/metabolismo
Isolamento Social
[Mh] Termos MeSH secundário: Animais
Aprendizagem da Esquiva/efeitos dos fármacos
Células Cultivadas
Feminino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Antagonistas Muscarínicos/farmacologia
Fibras Nervosas Mielinizadas/efeitos dos fármacos
Córtex Pré-Frontal/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Muscarinic Antagonists); 95QN29S1ID (Clemastine)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160122
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.3608-15.2016


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[PMID]:25482048
[Au] Autor:Apolloni S; Fabbrizio P; Parisi C; Amadio S; Volonté C
[Ad] Endereço:Cellular Biology and Neurobiology Institute, CNR, Via del Fosso di Fiorano, 65, 00143, Rome, Italy.
[Ti] Título:Clemastine Confers Neuroprotection and Induces an Anti-Inflammatory Phenotype in SOD1(G93A) Mouse Model of Amyotrophic Lateral Sclerosis.
[So] Source:Mol Neurobiol;53(1):518-531, 2016 Jan.
[Is] ISSN:1559-1182
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mutations in the Cu(2+)/Zn(2+) superoxide dismutase 1 (SOD1) gene underlie 14-23 % of familial and 1-7 % of sporadic cases of amyotrophic lateral sclerosis (ALS), a progressive neurodegenerative disease characterized by a specific loss of motor neurons in the brain and spinal cord. Neuroinflammation and oxidative stress are emerging as key players in the pathogenesis of ALS, thus justifying the interest in glial cells and particularly microglia, in addition to motor neurons, as novel therapeutic approaches against ALS. Recently, histamine was proven to participate in the pathogenesis of neuroinflammatory and neurodegenerative diseases, and particularly, microglia was shown to be sensitive to the histamine challenge mainly through histamine H1 receptors. Clemastine is a first-generation and CNS-penetrant H1 receptor antagonist considered as a safe antihistamine compound that was shown to possess immune suppressive properties. In order to investigate if clemastine might find promising application in the treatment of ALS, in this work, we tested its action in the SOD1(G93A) mouse model which is extensively used in ALS preclinical studies. We demonstrated that chronic clemastine administration in SOD1(G93A) mice reduces microgliosis, modulates microglia-related inflammatory genes, and enhances motor neuron survival. Moreover, in vitro, clemastine is able to modify several activation parameters of SOD1(G93A) microglia, and particularly CD68 and arginase-1 expression, as well as phospho-ERK1/2 and NADPH oxidase 2 levels. Being clemastine a drug already employed in clinical practice, our results strongly encourage its further exploitation as a candidate for preclinical trials and a new modulator of neuroinflammation in ALS.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/tratamento farmacológico
Esclerose Amiotrófica Lateral/genética
Clemastina/uso terapêutico
Modelos Animais de Doenças
Neuroproteção/efeitos dos fármacos
Superóxido Dismutase/genética
[Mh] Termos MeSH secundário: Esclerose Amiotrófica Lateral/enzimologia
Animais
Anti-Inflamatórios/farmacologia
Anti-Inflamatórios/uso terapêutico
Células Cultivadas
Clemastina/farmacologia
Feminino
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Microglia/efeitos dos fármacos
Microglia/enzimologia
Neuroproteção/fisiologia
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 95QN29S1ID (Clemastine); EC 1.15.1.1 (SOD1 G93A protein); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141209
[St] Status:MEDLINE
[do] DOI:10.1007/s12035-014-9019-8


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[PMID]:26291043
[Au] Autor:Zawrotniak M; Kozik A; Rapala-Kozik M
[Ad] Endereço:Department of Analytical Biochemistry, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University in Kraków, Kraków, Poland.
[Ti] Título:Selected mucolytic, anti-inflammatory and cardiovascular drugs change the ability of neutrophils to form extracellular traps (NETs).
[So] Source:Acta Biochim Pol;62(3):465-73, 2015.
[Is] ISSN:1734-154X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Neutrophils form the first line of host defense against infections that combat pathogens using two major mechanisms, the phagocytosis or the release of neutrophil extracellular traps (NETs). The netosis (NET formation) exerts additional, unfavorable effects on the fitness of host cells and is also involved at the sites of lung infection, increasing the mucus viscosity and in the circulatory system where it can influence the intravascular clot formation. Although molecular mechanisms underlying the netosis are still incompletely understood, a role of NADPH oxidase that activates the production of reactive oxygen species (ROS) during the initiation of NETs has been well documented. Since several commonly used drugs can affects the netosis, our current study was aimed to determine the effects of selected mucolytic, anti-inflammatory and cardiovascular drugs on NET formation, with a special emphasis on ROS production and NADPH oxidase activity. The treatment of neutrophils with N-acetylcysteine, ketoprofen and ethamsylate reduced the production of ROS by these cells in a dose-dependent manner. NET formation was also modulated by selected drugs. N-acetylcysteine inhibited the netosis but in the presence of H2O2 this neutrophil ability was restored, indicating that N-acetylcysteine may influence the NET formation by modulating ROS productivity. The administration of ethamsylate led to a significant reduction in NET formation and this effect was not restored by H2O2 or S. aureus, suggesting the unexpected additional side effects of this drug. Ketoprofen seemed to promote ROS-independent NET release, simultaneously inhibiting ROS production. The results, obtained in this study strongly suggest that the therapeutic strategies applied in many neutrophil-mediated diseases should take into account the NET-associated effects.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Fármacos Cardiovasculares/farmacologia
Armadilhas Extracelulares/efeitos dos fármacos
Armadilhas Extracelulares/metabolismo
Neutrófilos/efeitos dos fármacos
Neutrófilos/metabolismo
[Mh] Termos MeSH secundário: Acetilcisteína/química
Sobrevivência Celular
Clemastina/química
Relação Dose-Resposta a Droga
Etamsilato/química
Voluntários Saudáveis
Seres Humanos
Peróxido de Hidrogênio/química
Cetoprofeno/química
NADPH Oxidases/metabolismo
Fagocitose
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cardiovascular Agents); 0 (Reactive Oxygen Species); 24YL531VOH (Ethamsylate); 90Y4QC304K (Ketoprofen); 95QN29S1ID (Clemastine); BBX060AN9V (Hydrogen Peroxide); EC 1.6.3.- (NADPH Oxidases); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150821
[St] Status:MEDLINE
[do] DOI:10.18388/abp.2015_1055


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[PMID]:26253956
[Au] Autor:Li Z; He Y; Fan S; Sun B
[Ad] Endereço:Department of Neurology, Affiliated Hospital of Academy of Military Medical Sciences, Beijing, 100071, China. lizhifang@sohu.com.
[Ti] Título:Clemastine rescues behavioral changes and enhances remyelination in the cuprizone mouse model of demyelination.
[So] Source:Neurosci Bull;31(5):617-25, 2015 Oct.
[Is] ISSN:1995-8218
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Ab] Resumo:Increasing evidence suggests that white matter disorders based on myelin sheath impairment may underlie the neuropathological changes in schizophrenia. But it is unknown whether enhancing remyelination is a beneficial approach to schizophrenia. To investigate this hypothesis, we used clemastine, an FDA-approved drug with high potency in promoting oligodendroglial differentiation and myelination, on a cuprizone-induced mouse model of demyelination. The mice exposed to cuprizone (0.2% in chow) for 6 weeks displayed schizophrenia-like behavioral changes, including decreased exploration of the center in the open field test and increased entries into the arms of the Y-maze, as well as evident demyelination in the cortex and corpus callosum. Clemastine treatment was initiated upon cuprizone withdrawal at 10 mg/kg per day for 3 weeks. As expected, myelin repair was greatly enhanced in the demyelinated regions with increased mature oligodendrocytes (APC-positive) and myelin basic protein. More importantly, the clemastine treatment rescued the schizophrenia-like behavioral changes in the open field test and the Y-maze compared to vehicle, suggesting a beneficial effect via promoting myelin repair. Our findings indicate that enhancing remyelination may be a potential therapy for schizophrenia.
[Mh] Termos MeSH primário: Comportamento Animal/efeitos dos fármacos
Encéfalo/efeitos dos fármacos
Clemastina/administração & dosagem
Doenças Desmielinizantes/patologia
Bainha de Mielina/efeitos dos fármacos
Esquizofrenia/patologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/efeitos dos fármacos
Cuprizona/toxicidade
Doenças Desmielinizantes/induzido quimicamente
Doenças Desmielinizantes/complicações
Doenças Desmielinizantes/prevenção & controle
Modelos Animais de Doenças
Comportamento Exploratório/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Atividade Motora/efeitos dos fármacos
Proteína Básica da Mielina/metabolismo
Bainha de Mielina/metabolismo
Bainha de Mielina/fisiologia
Oligodendroglia/metabolismo
Esquizofrenia/induzido quimicamente
Esquizofrenia/complicações
Esquizofrenia/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Myelin Basic Protein); 5N16U7E0AO (Cuprizone); 95QN29S1ID (Clemastine)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150809
[St] Status:MEDLINE
[do] DOI:10.1007/s12264-015-1555-3


  9 / 296 MEDLINE  
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[PMID]:26219510
[Au] Autor:Lee SY; Jung JW; Kim TH; Kim HD
[Ad] Endereço:College of Pharmacy, Sookmyung Women's University, 53-12, Chungpa-Dong, Yongsan-Ku, Seoul, 140-742, Korea.
[Ti] Título:Asymmetric synthesis of H1 receptor antagonist (R,R)-clemastine.
[So] Source:Arch Pharm Res;38(12):2131-6, 2015 Dec.
[Is] ISSN:0253-6269
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:The first asymmetric synthesis of (R,R)-clemastine (1) has been accomplished by the coupling of (R)-tertiary alcohol 2 and (R)-chloroethylpyrrolidine 3 via O-alkylation. (R)-Tertiary alcohol 2 was synthesized by stereoselective alkylation of chiral α-benzyloxy ketone with Grignard reagent via chelation-controlled 1,4-asymmetric induction. In the reaction, chiral benzyl group acts as a chiral auxiliary as well as a protecting group. (R)-Chloroethylpyrrolidine 3 was prepared by asymmetric transformation starting with L-homoserine lactone, in which racemization-minimized N-allylation and ring-closing metathesis were involved as key steps.
[Mh] Termos MeSH primário: Química Farmacêutica/métodos
Clemastina/síntese química
Antagonistas dos Receptores Histamínicos H1/síntese química
Receptores Histamínicos H1/química
[Mh] Termos MeSH secundário: Estereoisomerismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Histamine H1 Antagonists); 0 (Receptors, Histamine H1); 95QN29S1ID (Clemastine)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:151202
[Lr] Data última revisão:
151202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150730
[St] Status:MEDLINE
[do] DOI:10.1007/s12272-015-0641-4


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[PMID]:25646708
[Au] Autor:Strassen U; Bas M; Hoffmann TK; Knopf A; Greve J
[Ad] Endereço:Department of Otorhinolaryngology, Head and Neck Surgery, Technical University of Munich, Munich, Germany.
[Ti] Título:Treatment of angiotensin receptor blocker-induced angioedema: A case series.
[So] Source:Laryngoscope;125(7):1619-23, 2015 Jul.
[Is] ISSN:1531-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Angiotensin II receptor antagonists have been proposed as a replacement therapy after the occurrence of either an angiotensin converting enzyme (ACE) inhibitor-induced angioedema or cough. However, recent studies indicate that angioedema is associated with elevated bradykinin levels in a small fraction of patients treated with angiotensin-II-receptor blockers, suggesting a common pathophysiological mechanism. To date, a standard treatment for angiotensin II receptor blocker-induced angioedema does not exist. METHODS: We present a case series of patients admitted to our hospital due to angioedema induced by an angiotensin II receptor blocker. The patients were either treated with either icatibant (n = 3) or prednisolone-21-hydrogen succinate/clemastine (n = 5). Both patient groups were compared with an untreated patient cohort (n = 3). All patients were previously diagnosed with essential hypertonia. RESULTS: Icatibant was an effective therapy for angiotensin II receptor blocker-induced angioedema. Full symptom recovery was achieved after 5 to 7 hours, whereas symptom remission occurred within 27 to 52 and 24 to 54 hours in patients treated with Solu-Decortin prednisolone/clemastine and untreated patients, respectively. The recovery time for icatibant was similar to that described in previous studies regarding the therapeutic efficacy of icatibant for the treatment of hereditary angioedema and patients suffering from angiotensin converting enzyme inhibitor-induced angioedema. CONCLUSIONS: Icatibant is a safe and effective substance for the treatment of angiotensin II receptor blocker-induced angioedema. Although the pathophysiology of angiotensin II receptor blocker-induced angioedema remains unclear, it appears to be associated with the bradykinin pathway.
[Mh] Termos MeSH primário: Angioedema/tratamento farmacológico
Antagonistas de Receptores de Angiotensina/efeitos adversos
Bradicinina/análogos & derivados
Clemastina/administração & dosagem
Prednisolona/análogos & derivados
[Mh] Termos MeSH secundário: Angioedema/induzido quimicamente
Antagonistas de Receptores de Angiotensina/uso terapêutico
Bradicinina/administração & dosagem
Antagonistas de Receptor B2 da Bradicinina/administração & dosagem
Relação Dose-Resposta a Droga
Quimioterapia Combinada
Hipertensão Essencial
Feminino
Seguimentos
Glucocorticoides/administração & dosagem
Antagonistas dos Receptores Histamínicos H1/administração & dosagem
Seres Humanos
Hipertensão/tratamento farmacológico
Injeções Intravenosas
Masculino
Prednisolona/administração & dosagem
Estudos Retrospectivos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin Receptor Antagonists); 0 (Bradykinin B2 Receptor Antagonists); 0 (Glucocorticoids); 0 (Histamine H1 Antagonists); 7PG89G35Q7 (icatibant); 95QN29S1ID (Clemastine); 9PHQ9Y1OLM (Prednisolone); G7080T74ON (prednisolone hemisuccinate); S8TIM42R2W (Bradykinin)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150204
[St] Status:MEDLINE
[do] DOI:10.1002/lary.25163



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