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[PMID]:28448889
[Au] Autor:Yang A; Chen J; Ma Y; Wang L; Fan Y; He X
[Ad] Endereço:School of Chinese Materia Medica, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, PR China; Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin, 300193, PR China.
[Ti] Título:Studies on the metabolites difference of psoralen/isopsoralen in human and six mammalian liver microsomes in vitro by UHPLC-MS/MS.
[So] Source:J Pharm Biomed Anal;141:200-209, 2017 Jul 15.
[Is] ISSN:1873-264X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Psoralen and isopsoralen are found in many fruits, vegetables and traditional Chinese medicines (TCM), such as Ficus carica L., Celery, Fructus Psoraleae etc. Modern pharmacological studies found that psoralen and isopsoralen can show estrogen-like activity, antitumor, and antibacterial activities etc. However, some research results also show some liver damage associated with the use of psoralen/isopsoralen or related medicines in human. Many studies focus on the pharmacological activities of psoralen/isopsoralen, while it is important to choose the suitable pharmacological models which are relevant to human in drug metabolism and pharmacokinetic process. The aim of this study is to identify the metabolites of psoralen/isopsoralen by human and six mammalian liver microsomes, and compare the metabolites difference of different species. Psoralen/isopsoralen are metabolized by liver microsomes of different animals to form five and seven metabolites, respectively. The metabolism of psoralen/isopsoralen undergoes hydroxylation, hydrogenation and hydrolysis, and oxidation of the furan ring to generate a furanoepoxide or γ-ketoenal intermediate. Furanoepoxide then forms a dihydrodiol, while γ-ketoenal forms 6-(7-hydroxycoumaryl)-acetic acid (in psoralen)/8-(7-hydroxycoumaryl)-acetic acid (in isopsoralen). By comparing the types of metabolites in the seven liver microsomes, it shows that the metabolic behaviors of psoralen by Beagle dog is most relevant to human, while the metabolic behaviors of isopsoralen by Sprague-Dawley rat is most similar to human. By comparing the relative amounts of the main metabolites, it shows that the metabolic capabilities of Sprague-Dawley rat and Rhesus monkey for psoralen are most similar to human, while the metabolic capabilities of Mouse, Dunkin-Hartley guinea pig, Sprague-Dawley rat, and human for isopsoralen are similar. Furthermore, the results show that the metabolic capability of human for psoralen and isopsoralen are weaker than other mammal species. The results of this work are useful for studying the metabolism mechanism of psoralen/isopsolaren, and choosing the most relevant animal species for investigation of psoralen/isopsolaren from experimental animals to human.
[Mh] Termos MeSH primário: Microssomos Hepáticos
[Mh] Termos MeSH secundário: Animais
Cromatografia Líquida de Alta Pressão
Ficusina
Furocumarinas
Seres Humanos
Ratos Sprague-Dawley
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Furocoumarins); CZZ080D7BD (angelicin); KTZ7ZCN2EX (Ficusin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180125
[Lr] Data última revisão:
180125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE


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[PMID]:28833022
[Au] Autor:Dawe RS
[Ad] Endereço:Photobiology Unit, Department of Dermatology, Ninewells Hospital and Medical School, Dundee, DD1 9SY, U.K.
[Ti] Título:Maintenance therapy with psoralen-ultraviolet A for mycosis fungoides: in the absence of evidence sitting on the fence is appropriate.
[So] Source:Br J Dermatol;177(2):337-338, 2017 08.
[Is] ISSN:1365-2133
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Ficusina
Micose Fungoide
[Mh] Termos MeSH secundário: Seres Humanos
Terapia PUVA
Neoplasias Cutâneas
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
KTZ7ZCN2EX (Ficusin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1111/bjd.15673


  3 / 837 MEDLINE  
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[PMID]:28833012
[Au] Autor:Vieyra-Garcia P; Wolf P
[Ad] Endereço:Department of Dermatology, Medical University of Graz, Graz, Austria.
[Ti] Título:Psoralen-ultraviolet A maintenance in mycosis fungoides: the underlying question.
[So] Source:Br J Dermatol;177(2):336-337, 2017 08.
[Is] ISSN:1365-2133
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Ficusina
Micose Fungoide
[Mh] Termos MeSH secundário: Seres Humanos
Terapia PUVA
Neoplasias Cutâneas
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
KTZ7ZCN2EX (Ficusin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1111/bjd.15670


  4 / 837 MEDLINE  
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[PMID]:28753523
[Au] Autor:Doppalapudi S; Mahira S; Khan W
[Ad] Endereço:Department of Pharmaceutics, National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad 500037, India.
[Ti] Título:Development and in vitro assessment of psoralen and resveratrol co-loaded ultradeformable liposomes for the treatment of vitiligo.
[So] Source:J Photochem Photobiol B;174:44-57, 2017 Sep.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Vitiligo is a de-pigmenting skin disorder characterized by white patches on skin due to partial or complete loss of melanocytes. Psoralen in combination with ultraviolet-A (PUVA) acts by stimulation of melanin content and tyrosinase activity in melanocytes. Resveratrol, a sirtuin activator and a potential anti-oxidant reduce oxidative stress which is one of the triggering factors for initiation of vitiligo. Despite their therapeutic activity, weak percutaneous permeability of psoralen and poor solubility of resveratrol hinders their effective topical administration. The aim of present study is to formulate ultradeformable liposomes (UDL) co-loaded with psoralen and resveratrol for evaluation of PUVA and anti-oxidant combination in vitiligo treatment. For this purpose, UDL composed of DC-Chol, cholesterol and sodium deoxy cholate were prepared for their co-delivery. Liposomal carriers were characterized and evaluated for their efficacy using B16F10 cell line. Free radical scavenging potential was also determined for these carriers by in vitro anti-oxidant assays. Optimal co-loaded UDL with particle size ranging from 120 to 130nm, zeta potential of +46.2mV, entrapment efficiency of 74.09% (psoralen) and 76.91% (resveratrol) were obtained. Compared to control, co-loaded UDL showed significant stimulation of melanin and tyrosinase activity with major contribution of psoralen. Further, co-loaded UDL also exhibited potential free radical scavenging activity where resveratrol played a key role. Hence, psoralen and resveratrol co-loaded UDL acts in vitiligo through dual mechanisms of action viz., stimulation of melanin and tyrosinase activity as well as by anti-oxidant activity. These findings indicate that psoralen and resveratrol co-loaded UDL has the promising therapeutic potential for the treatment of vitiligo.
[Mh] Termos MeSH primário: Ficusina/química
Ficusina/farmacologia
Estilbenos/química
Estilbenos/farmacologia
Vitiligo/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Transporte Biológico
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Composição de Medicamentos
Liberação Controlada de Fármacos
Ficusina/metabolismo
Ficusina/uso terapêutico
Cinética
Lipossomos
Melaninas/metabolismo
Camundongos
Monofenol Mono-Oxigenase/metabolismo
Tamanho da Partícula
Estilbenos/metabolismo
Estilbenos/uso terapêutico
Vitiligo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Liposomes); 0 (Melanins); 0 (Stilbenes); EC 1.14.18.1 (Monophenol Monooxygenase); KTZ7ZCN2EX (Ficusin); Q369O8926L (resveratrol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE


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[PMID]:28349059
[Au] Autor:Chen S; Wang Y; Yang Y; Xiang T; Liu J; Zhou H; Wu X
[Ad] Endereço:Department of Traditional Chinese Medicine, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China.
[Ti] Título:Psoralen Inhibited Apoptosis of Osteoporotic Osteoblasts by Modulating IRE1-ASK1-JNK Pathway.
[So] Source:Biomed Res Int;2017:3524307, 2017.
[Is] ISSN:2314-6141
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Osteoporosis is a common disease causing fracture in older populations. Abnormal apoptosis of osteoblasts contributes to the genesis of osteoporosis. Inhibiting apoptosis of osteoblasts provides a promising strategy to prevent osteoporosis. The proliferation of osteoblasts isolated from osteoporotic patients or healthy subjects was determined by MTT assay. Apoptosis was determined by Annexin V/PI assay. Protein expression was measured by western blot. The proliferation of osteoblasts isolated from osteoporotic patients was inhibited and the apoptosis level of these cells was higher than the osteoblasts from healthy subjects. Incubation with psoralen or estradiol significantly enhanced the proliferation and decreased the apoptosis level of osteoporotic osteoblasts. Western blot demonstrated that psoralen or estradiol treatment downregulated the expression of IRE1, p-ASK, p-JNK, and Bax. Meanwhile, expression of Bcl-2 was upregulated. Pretreatment by IRE1 agonist tunicamycin or JNK agonist anisomycin attenuated the effect of psoralen on osteoporotic osteoblasts. Psoralen inhibited apoptosis of osteoporotic osteoblasts by regulating IRE1-ASK1-JNK pathway.
[Mh] Termos MeSH primário: Endorribonucleases/genética
Ficusina/administração & dosagem
MAP Quinase Quinase 4/genética
MAP Quinase Quinase Quinase 5/genética
Osteoporose/tratamento farmacológico
Proteínas Serina-Treonina Quinases/genética
[Mh] Termos MeSH secundário: Anisomicina/administração & dosagem
Apoptose/efeitos dos fármacos
Diferenciação Celular/genética
Proliferação Celular/efeitos dos fármacos
Endorribonucleases/biossíntese
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
MAP Quinase Quinase 4/biossíntese
MAP Quinase Quinase Quinase 5/biossíntese
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Meia-Idade
Osteoblastos/efeitos dos fármacos
Osteoporose/genética
Osteoporose/patologia
Cultura Primária de Células
Proteínas Serina-Treonina Quinases/biossíntese
Proteínas Proto-Oncogênicas c-bcl-2/biossíntese
Tunicamicina/administração & dosagem
Proteína X Associada a bcl-2/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-bcl-2); 0 (bcl-2-Associated X Protein); 11089-65-9 (Tunicamycin); 6C74YM2NGI (Anisomycin); EC 2.7.11.1 (ERN1 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.25 (MAP Kinase Kinase Kinase 5); EC 2.7.11.25 (MAP3K5 protein, human); EC 2.7.12.2 (MAP Kinase Kinase 4); EC 3.1.- (Endoribonucleases); KTZ7ZCN2EX (Ficusin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170428
[Lr] Data última revisão:
170428
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.1155/2017/3524307


  6 / 837 MEDLINE  
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[PMID]:28219011
[Au] Autor:Buchman CD; Hurley TD
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Indiana University School of Medicine , Indianapolis, Indiana 46202, United States.
[Ti] Título:Inhibition of the Aldehyde Dehydrogenase 1/2 Family by Psoralen and Coumarin Derivatives.
[So] Source:J Med Chem;60(6):2439-2455, 2017 Mar 23.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aldehyde dehydrogenase 2 (ALDH2), one of 19 ALDH superfamily members, catalyzes the NAD -dependent oxidation of aldehydes to their respective carboxylic acids. In this study, we further characterized the inhibition of four psoralen and coumarin derivatives toward ALDH2 and compared them to the ALDH2 inhibitor daidzin for selectivity against five ALDH1/2 isoenzymes. Compound 2 (K = 19 nM) binds within the aldehyde-binding site of the free enzyme species of ALDH2. Thirty-three structural analogs were examined to develop a stronger SAR profile. Seven compounds maintained or improved upon the selectivity toward one of the five ALDH1/2 isoenzymes, including compound 36, a selective inhibitor for ALDH2 (K = 2.4 µM), and compound 32, which was 10-fold selective for ALDH1A1 (K = 1.2 µM) versus ALDH1A2. Further medicinal chemistry on the compounds' basic scaffold could enhance the potency and selectivity for ALDH1A1 or ALDH2 and generate chemical probes to examine the unique and overlapping functions of the ALDH1/2 isoenzymes.
[Mh] Termos MeSH primário: Aldeído-Desidrogenase Mitocondrial/antagonistas & inibidores
Aldeído Desidrogenase/antagonistas & inibidores
Cumarínicos/farmacologia
Inibidores Enzimáticos/farmacologia
Ficusina/farmacologia
Isoenzimas/antagonistas & inibidores
Retinal Desidrogenase/antagonistas & inibidores
[Mh] Termos MeSH secundário: Aldeído Desidrogenase/química
Aldeído Desidrogenase/metabolismo
Aldeído-Desidrogenase Mitocondrial/metabolismo
Cumarínicos/química
Desenho de Drogas
Inibidores Enzimáticos/química
Ficusina/química
Seres Humanos
Isoenzimas/metabolismo
Simulação de Acoplamento Molecular
Retinal Desidrogenase/química
Retinal Desidrogenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Coumarins); 0 (Enzyme Inhibitors); 0 (Isoenzymes); EC 1.2.1.- (aldehyde dehydrogenase 1); EC 1.2.1.3 (ALDH1A1 protein, human); EC 1.2.1.3 (Aldehyde Dehydrogenase); EC 1.2.1.3 (Aldehyde Dehydrogenase, Mitochondrial); EC 1.2.1.36 (ALDH1A2 protein, human); EC 1.2.1.36 (Retinal Dehydrogenase); KTZ7ZCN2EX (Ficusin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170221
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.6b01825


  7 / 837 MEDLINE  
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[PMID]:27258736
[Au] Autor:Bishnoi A; Parsad D; Vinay K; Kumaran MS
[Ad] Endereço:Department of Dermatology, Venereology and Leprology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
[Ti] Título:Phototherapy using narrowband ultraviolet B and psoralen plus ultraviolet A is beneficial in steroid-dependent antihistamine-refractory chronic urticaria: a randomized, prospective observer-blinded comparative study.
[So] Source:Br J Dermatol;176(1):62-70, 2017 Jan.
[Is] ISSN:1365-2133
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Literature on the efficacy of phototherapy in steroid-dependent antihistamine-refractory chronic urticaria (CRU) is limited. OBJECTIVES: To assess and compare the efficacy of psoralen plus ultraviolet A (PUVA) and narrowband ultraviolet B (NB-UVB) in steroid-dependent CRU. METHODS: In this randomized, prospective observer-blinded comparative study, 50 patients with steroid-dependent CRU (6 months of spontaneous urticaria with no response after 3 consecutive months of antihistamines and steroid dependence) were administered either PUVA (group A) or NB-UVB (group B) for 90 days, with a post-treatment follow-up of 90 days. The treatment efficacy was assessed using the average urticaria activity score 7 (aUAS7) and outcome scoring scale (OSS) every 2 weeks. RESULTS: The mean values of aUAS7 progressively decreased from 4·9 ± 0·8 and 5·0 ± 0·7 at baseline to 1·9 ± 0·7 and 1·4 ± 0·7 in groups A and B, respectively, by day 90. This further decreased to 1·5 ± 0·8 and 1·4 ± 1·0 at day 180 in both groups. The values of OSS progressively increased from baseline (1·6 ± 0·5 in group A and 1·3 ± 0·5 in group B) to 3·9 ± 0·3 and 4·0 ± 0·3 in groups A and B, respectively, by day 90, and 3·9 ± 0·5 and 4·0 ± 0·6 by day 180. NB-UVB fared statistically better than PUVA at different time points. Adverse events encountered were minimal and did not warrant treatment discontinuation. CONCLUSIONS: Phototherapy, especially NB-UVB, is an effective, safe and affordable therapeutic modality for steroid-dependent CRU and should be tried prior to third-line treatment options such as omalizumab, ciclosporin and other immunosuppressants.
[Mh] Termos MeSH primário: Ficusina/uso terapêutico
Fármacos Fotossensibilizantes/uso terapêutico
Terapia Ultravioleta/métodos
Urticária/tratamento farmacológico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Análise de Variância
Doença Crônica
Resistência a Medicamentos
Feminino
Antagonistas dos Receptores Histamínicos/uso terapêutico
Seres Humanos
Masculino
Meia-Idade
Satisfação do Paciente
Estudos Prospectivos
Método Simples-Cego
Testes Cutâneos
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Histamine Antagonists); 0 (Photosensitizing Agents); KTZ7ZCN2EX (Ficusin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160604
[St] Status:MEDLINE
[do] DOI:10.1111/bjd.14778


  8 / 837 MEDLINE  
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[PMID]:27911399
[Au] Autor:Mukherjee A; Vasquez KM
[Ad] Endereço:Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin.
[Ti] Título:Tools to Study the Role of Architectural Protein HMGB1 in the Processing of Helix Distorting, Site-specific DNA Interstrand Crosslinks.
[So] Source:J Vis Exp;(117), 2016 Nov 10.
[Is] ISSN:1940-087X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:High mobility group box 1 (HMGB1) protein is a non-histone architectural protein that is involved in regulating many important functions in the genome, such as transcription, DNA replication, and DNA repair. HMGB1 binds to structurally distorted DNA with higher affinity than to canonical B-DNA. For example, we found that HMGB1 binds to DNA interstrand crosslinks (ICLs), which covalently link the two strands of the DNA, cause distortion of the helix, and if left unrepaired can cause cell death. Due to their cytotoxic potential, several ICL-inducing agents are currently used as chemotherapeutic agents in the clinic. While ICL-forming agents show preferences for certain base sequences (e.g., 5'-TA-3' is the preferred crosslinking site for psoralen), they largely induce DNA damage in an indiscriminate fashion. However, by covalently coupling the ICL-inducing agent to a triplex-forming oligonucleotide (TFO), which binds to DNA in a sequence-specific manner, targeted DNA damage can be achieved. Here, we use a TFO covalently conjugated on the 5' end to a 4'-hydroxymethyl-4,5',8-trimethylpsoralen (HMT) psoralen to generate a site-specific ICL on a mutation-reporter plasmid to use as a tool to study the architectural modification, processing, and repair of complex DNA lesions by HMGB1 in human cells. We describe experimental techniques to prepare TFO-directed ICLs on reporter plasmids, and to interrogate the association of HMGB1 with the TFO-directed ICLs in a cellular context using chromatin immunoprecipitation assays. In addition, we describe DNA supercoiling assays to assess specific architectural modification of the damaged DNA by measuring the amount of superhelical turns introduced on the psoralen-crosslinked plasmid by HMGB1. These techniques can be used to study the roles of other proteins involved in the processing and repair of TFO-directed ICLs or other targeted DNA damage in any cell line of interest.
[Mh] Termos MeSH primário: Proteína HMGB1
[Mh] Termos MeSH secundário: Reagentes para Ligações Cruzadas
DNA
Dano ao DNA
Reparo do DNA
Ficusina
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Nm] Nome de substância:
0 (Cross-Linking Reagents); 0 (HMGB1 Protein); 9007-49-2 (DNA); KTZ7ZCN2EX (Ficusin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161203
[St] Status:MEDLINE
[do] DOI:10.3791/54678


  9 / 837 MEDLINE  
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[PMID]:27713014
[Au] Autor:Niu C; Pang GX; Li G; Dou J; Nie LF; Himit H; Kabas M; Aisa HA
[Ad] Endereço:The Key Laboratory of Plant Resources and Chemistry of Arid Zone, Chinese Academy of Sciences, Urumqi 830011, China; State Key Laboratory Basis of Xinjiang Indigenous Medicinal Plants Resource Utilization, Xinjiang Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Urumqi 830
[Ti] Título:Synthesis and biological evaluation of furocoumarin derivatives on melanin synthesis in murine B16 cells for the treatment of vitiligo.
[So] Source:Bioorg Med Chem;24(22):5960-5968, 2016 Nov 15.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Furocoumarins, isolated from Psoralen corylifolia L., were found to be the most effective drug in the treatment of vitiligo nowadays. Twenty-five furocoumarin derivatives were thus designed and synthesized in order to improve the melanogenesis in B16 cells for the first time. Among them, twenty-three compounds were more potent than the positive control (8-MOP), the commonly used drug for vitiligo in clinic. Noticeably, compounds 6m (350.5%) and 6p (313.1%) based on the scaffold of 6k (2H-benzofuro[2,3-h]chromen-2-one) were nearly 3-fold stronger than 8-MOP (114.50%). The in vitro melanin synthesis evaluation of these structurally diverse analogues had also led to an outline of structure-activity relationship.
[Mh] Termos MeSH primário: Furocumarinas/farmacologia
Melaninas/antagonistas & inibidores
Vitiligo/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Relação Dose-Resposta a Droga
Ficusina/química
Furocumarinas/química
Furocumarinas/isolamento & purificação
Melaninas/biossíntese
Camundongos
Estrutura Molecular
Relação Estrutura-Atividade
Vitiligo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Furocoumarins); 0 (Melanins); KTZ7ZCN2EX (Ficusin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161008
[St] Status:MEDLINE


  10 / 837 MEDLINE  
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[PMID]:27693351
[Au] Autor:Semlow DR; Zhang J; Budzowska M; Drohat AC; Walter JC
[Ad] Endereço:Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
[Ti] Título:Replication-Dependent Unhooking of DNA Interstrand Cross-Links by the NEIL3 Glycosylase.
[So] Source:Cell;167(2):498-511.e14, 2016 Oct 06.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During eukaryotic DNA interstrand cross-link (ICL) repair, cross-links are resolved ("unhooked") by nucleolytic incisions surrounding the lesion. In vertebrates, ICL repair is triggered when replication forks collide with the lesion, leading to FANCI-FANCD2-dependent unhooking and formation of a double-strand break (DSB) intermediate. Using Xenopus egg extracts, we describe here a replication-coupled ICL repair pathway that does not require incisions or FANCI-FANCD2. Instead, the ICL is unhooked when one of the two N-glycosyl bonds forming the cross-link is cleaved by the DNA glycosylase NEIL3. Cleavage by NEIL3 is the primary unhooking mechanism for psoralen and abasic site ICLs. When N-glycosyl bond cleavage is prevented, unhooking occurs via FANCI-FANCD2-dependent incisions. In summary, we identify an incision-independent unhooking mechanism that avoids DSB formation and represents the preferred pathway of ICL repair in a vertebrate cell-free system.
[Mh] Termos MeSH primário: Quebras de DNA de Cadeia Dupla
Reparo do DNA
Replicação do DNA
Proteína do Grupo de Complementação D2 da Anemia de Fanconi/metabolismo
Proteínas de Grupos de Complementação da Anemia de Fanconi/metabolismo
N-Glicosil Hidrolases/metabolismo
[Mh] Termos MeSH secundário: Animais
Sistema Livre de Células/química
Reagentes para Ligações Cruzadas/química
DNA/biossíntese
DNA/química
Proteína do Grupo de Complementação D2 da Anemia de Fanconi/química
Proteínas de Grupos de Complementação da Anemia de Fanconi/química
Ficusina/química
N-Glicosil Hidrolases/química
Xenopus laevis
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cross-Linking Reagents); 0 (Fanconi Anemia Complementation Group D2 Protein); 0 (Fanconi Anemia Complementation Group Proteins); 9007-49-2 (DNA); EC 3.2.2.- (N-Glycosyl Hydrolases); KTZ7ZCN2EX (Ficusin)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161004
[St] Status:MEDLINE



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