Base de dados : MEDLINE
Pesquisa : D03.132.098 [Categoria DeCS]
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  1 / 1517 MEDLINE  
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[PMID]:29199255
[Au] Autor:Tanahashi T
[Ad] Endereço:Kobe Pharmaceutical University.
[Ti] Título:[Diversity of Secondary Metabolites from Some Medicinal Plants and Cultivated Lichen Mycobionts].
[So] Source:Yakugaku Zasshi;137(12):1443-1482, 2017.
[Is] ISSN:1347-5231
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:Studies on the structural determination, biosynthesis, and biological activities of secondary metabolites from natural sources are significant in the field of natural products chemistry. This review focuses on diverse secondary metabolites isolated from medicinal plants and cultivated mycobionts of lichens in our laboratory. Monoterpene-tetrahydroisoquinoline glycosides and alkaloids isolated from Cephaelis acuminata and Alangium lamarckii gave important information on the biosynthesis of ipecac alkaloids. A variety of glycosides linked with a secologanin unit and indole alkaloids were obtained from medicinal plants belonging to the families of Rubiaceae, Apocynaceae, and Loganiaceae. Plant species of the four genera Fraxinus, Syringa, Jasminum, and Ligustrum of the family Oleaceae were chemically investigated to provide several types of secoiridoid and iridoid glucosides. The biosynthetic pathway leading from protopine to benzophenanthridine alkaloids in suspension cell cultures of Eschscholtzia californica was elucidated. The structures and biological activities of the bisbenzylisoquinoline alkaloids of Stephania cepharantha and Nelumbo nucifera were also investigated. In addition, the mycobionts of lichens were cultivated to afford various types of metabolites that differ from the lichen substances of intact lichens but are structurally similar to fungal metabolites. The biosynthetic origins of some metabolites were also studied. These findings suggest that cultures of lichen mycobionts could be sources of new bioactive compounds and good systems for investigating secondary metabolism in lichens.
[Mh] Termos MeSH primário: Alcaloides/isolamento & purificação
Glicosídeos/isolamento & purificação
Líquens/metabolismo
Plantas Medicinais/metabolismo
[Mh] Termos MeSH secundário: Alangiaceae/metabolismo
Alcaloides/biossíntese
Alcaloides/química
Benzilisoquinolinas
Cephaelis/metabolismo
Eschscholzia/metabolismo
Glicosídeos/biossíntese
Glicosídeos/química
Iridoides
Monoterpenos
Oleaceae/metabolismo
Rubiaceae/metabolismo
Stephania/metabolismo
Tetra-Hidroisoquinolinas
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Alkaloids); 0 (Benzylisoquinolines); 0 (Glycosides); 0 (Iridoids); 0 (Monoterpenes); 0 (Tetrahydroisoquinolines); 56W89FBX3E (1,2,3,4-tetrahydroisoquinoline)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.1248/yakushi.17-00147


  2 / 1517 MEDLINE  
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[PMID]:29197576
[Au] Autor:Xu T; Singh D; Liu J; Li H; Peng S; Rizzolo LJ; Wang SB
[Ad] Endereço:Aier School of Ophthalmology, Central South University, Changsha, China; Dept. of Surgery, Yale University School of Medicine, New Haven, CT, USA; Dept. of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, CT, USA.
[Ti] Título:Neferine, is not inducer but blocker for macroautophagic flux targeting on lysosome malfunction.
[So] Source:Biochem Biophys Res Commun;495(1):1516-1521, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neferine, an alkaloid isolated from Lotus seeds, displays multiple pharmacological effects that counter cancer, oxidants, and arrhythmia. It was initially identified as a strong inducer for macroautophagy in cancer cells by suppressing AMPK/mTOR signaling. In this study, we found that autophagy signaling was inhibited in the condition of neferine treatment. Exposure to neferine resulted in the accumulation of LC3-II and an associated adaptor protein, p62/SQSTM1. Knockdown of ATG5 failed to reduce the accumulation of LC3-II induced by neferine. The electron microscopy (EM) images showed that neferine induce accumulation of multi-vesicle bodies (MVB) and failure of lysosome maturation. Moreover, exposure to neferine reduced maturation of cathepsin D and impaired the degradation of autophagic and phagocytic cargos. Rather than stimulate autophagic flux, the data indicate that neferine impaired lysosomes to block degradation within phagolysosomes.
[Mh] Termos MeSH primário: Autofagia/efeitos dos fármacos
Autofagia/fisiologia
Benzilisoquinolinas/administração & dosagem
Lisossomos/fisiologia
Lisossomos/ultraestrutura
Proteínas Associadas aos Microtúbulos/metabolismo
[Mh] Termos MeSH secundário: Antioxidantes/administração & dosagem
Relação Dose-Resposta a Droga
Células HEK293
Células HeLa
Seres Humanos
Lisossomos/efeitos dos fármacos
Análise do Fluxo Metabólico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Benzylisoquinolines); 0 (MAP1LC3A protein, human); 0 (Microtubule-Associated Proteins); 2292-16-2 (neferine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171204
[St] Status:MEDLINE


  3 / 1517 MEDLINE  
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[PMID]:29024815
[Au] Autor:Tang ZH; Cao WX; Guo X; Dai XY; Lu JH; Chen X; Zhu H; Lu JJ
[Ad] Endereço:State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.
[Ti] Título:Identification of a novel autophagic inhibitor cepharanthine to enhance the anti-cancer property of dacomitinib in non-small cell lung cancer.
[So] Source:Cancer Lett;412:1-9, 2018 Jan 01.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Inhibition of autophagy is a promising strategy for non-small cell lung cancer (NSCLC) treatment, which is in the clinical trials. However, only chloroquine is used in clinic as an autophagic inhibitor and the inhibitory effect of chloroquine on autophagy is finite. Therefore, the development of an alternative autophagic inhibitor for NSCLC therapy becomes necessary. In the present study, cepharanthine (CEP), an alkaloid extracted from Stephania cepharantha Hayata, was identified as a novel autophagic inhibitor in NSCLC cells. The potential mechanism of the CEP-inhibited autophagy was by blockage of autophagosome-lysosome fusion and inhibition of lysosomal cathepsin B and cathepsin D maturation. Furthermore, we found for the first time that dacomitinib (DAC), a second-generation epidermal growth factor receptor inhibitor that in the phase III clinical trials for NSCLC treatment, induced a protective autophagy to decrease its anti-cancer effect. Combined treatment with CEP increased the anti-proliferative and apoptotic effects of DAC in vitro and enhanced the anti-cancer effect of DAC in NCI-H1975 xenograft mice. Collectively, CEP might be further developed as an autophagic inhibitor, and combined treatment of CEP and DAC could offer an effective strategy for NSCLC treatment.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Autofagia/efeitos dos fármacos
Benzilisoquinolinas/farmacologia
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Neoplasias Pulmonares/tratamento farmacológico
Quinazolinonas/farmacologia
[Mh] Termos MeSH secundário: Animais
Carcinoma Pulmonar de Células não Pequenas/patologia
Catepsinas/metabolismo
Linhagem Celular Tumoral
Seres Humanos
Concentração de Íons de Hidrogênio
Neoplasias Pulmonares/patologia
Camundongos
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Benzylisoquinolines); 0 (PF 00299804); 0 (Quinazolinones); 7592YJ0J6T (cepharanthine); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.4.- (Cathepsins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171205
[Lr] Data última revisão:
171205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE


  4 / 1517 MEDLINE  
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[PMID]:29061791
[Au] Autor:Liu KC; Lin YJ; Hsiao YT; Lin ML; Yang JL; Huang YP; Chu YL; Chung JG
[Ad] Endereço:Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan, R.O.C.
[Ti] Título:Tetrandrine Induces Apoptosis in Human Nasopharyngeal Carcinoma NPC-TW 039 Cells by Endoplasmic Reticulum Stress and Ca /Calpain Pathways.
[So] Source:Anticancer Res;37(11):6107-6118, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Tetrandrine is an alkaloid extracted from a traditional China medicine plant, and is considered part of food therapy as well. In addition, it has been widely reported to induce apoptotic cell death in many human cancer cells. However, the mechanism of Tetrandrine on human nasopharyngeal carcinoma cells (NPC) is still questioned. In our study, we examined whether Tetrandrine can induce apoptosis of NPC-TW 039 cells. We found that cell morphology was changed after treatment with different concentrations of Tetrandrine. Further, we indicated that the NPC-TW 039 cells viability decreased in a Tetrandrine dose-dependent manner. We also found that tetrandrine induced cell cycle arrest in G /G phase. Tetrandrine induced DNA condensation by DAPI staining as well. In addition, we found that Tetrandrine induced Ca release in the cytosol. At the same time, endoplasmic reticulum (ER) stress occurred. Then we used western blotting to examine the protein expression which is associated with mitochondria-mediated apoptotic pathways and caspase-dependent pathways. To further examine whether Ca was released or not with Tetrandrine induced-apoptosis, we used the chelator of Ca and showed that cell viability increased. At the same time, caspase-3 expression was decreased. Furthermore, confocal microscopy examination revealed that Tetrandrine induced expression of ER stress-related proteins GADD153 and GRP78. Our results indicate that Tetrandrine induces apoptosis through calcium-mediated ER stress and caspase pathway in NPC-TW 039 cells. In conclusion, Tetrandrine may could be used for treatment of human nasopharyngeal carcinoma in future.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia
Benzilisoquinolinas/farmacologia
Cálcio/metabolismo
Calpaína/metabolismo
Carcinoma/patologia
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Neoplasias Nasofaríngeas/patologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Carcinoma/tratamento farmacológico
Carcinoma/metabolismo
Ciclo Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Seres Humanos
Masculino
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Meia-Idade
Neoplasias Nasofaríngeas/tratamento farmacológico
Neoplasias Nasofaríngeas/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Benzylisoquinolines); 0 (Reactive Oxygen Species); 29EX23D5AJ (tetrandrine); EC 3.4.22.- (Calpain); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE


  5 / 1517 MEDLINE  
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[PMID]:28923401
[Au] Autor:Lyu J; Yang EJ; Head SA; Ai N; Zhang B; Wu C; Li RJ; Liu Y; Yang C; Dang Y; Kwon HJ; Ge W; Liu JO; Shim JS
[Ad] Endereço:Faculty of Health Sciences, University of Macau, Taipa, Macau SAR, China.
[Ti] Título:Pharmacological blockade of cholesterol trafficking by cepharanthine in endothelial cells suppresses angiogenesis and tumor growth.
[So] Source:Cancer Lett;409:91-103, 2017 Nov 28.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Cholesterol is an important modulator of membrane protein function and signaling in endothelial cells, thus making it an emerging target for anti-angiogenic agents. In this study, we employed a phenotypic screen that detects intracellular cholesterol distribution in endothelial cells (HUVEC) and identified 13 existing drugs as cholesterol trafficking inhibitors. Cepharanthine, an approved drug for anti-inflammatory and cancer management use, was amongst the candidates, which was selected for in-depth mechanistic studies to link cholesterol trafficking and angiogenesis. Cepharanthine inhibited the endolysosomal trafficking of free-cholesterol and low-density lipoprotein in HUVEC by binding to Niemann-Pick disease, type C1 (NPC1) protein and increasing the lysosomal pH. The blockade of cholesterol trafficking led to a cholesterol-dependent dissociation of mTOR from the lysosomes and inhibition of its downstream signaling. Cepharanthine inhibited angiogenesis in HUVEC and in zebrafish in a cholesterol-dependent manner. Furthermore, cepharanthine suppressed tumor growth in vivo by inhibiting angiogenesis and it enhanced the antitumor activity of the standard chemotherapy cisplatin in lung and breast cancer xenografts in mice. Altogether, these results strongly support the idea that cholesterol trafficking is a viable drug target for anti-angiogenesis and that the inhibitors identified among existing drugs, such as cepharanthine, could be potential anti-angiogenic and antitumor agents.
[Mh] Termos MeSH primário: Benzilisoquinolinas/farmacologia
Colesterol/metabolismo
Neoplasias/irrigação sanguínea
Neoplasias/tratamento farmacológico
Neovascularização Patológica/tratamento farmacológico
[Mh] Termos MeSH secundário: Inibidores da Angiogênese/farmacologia
Animais
Animais Geneticamente Modificados
Antineoplásicos Fitogênicos/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Benzilisoquinolinas/administração & dosagem
Processos de Crescimento Celular/efeitos dos fármacos
Cisplatino/administração & dosagem
Cisplatino/farmacologia
Sinergismo Farmacológico
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Lisossomos/efeitos dos fármacos
Lisossomos/metabolismo
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Neoplasias/metabolismo
Neoplasias/patologia
Neovascularização Patológica/metabolismo
Neovascularização Patológica/patologia
Microambiente Tumoral/efeitos dos fármacos
Ensaios Antitumorais Modelo de Xenoenxerto
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Antineoplastic Agents, Phytogenic); 0 (Benzylisoquinolines); 7592YJ0J6T (cepharanthine); 97C5T2UQ7J (Cholesterol); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE


  6 / 1517 MEDLINE  
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[PMID]:28754437
[Au] Autor:Lee HS; Safe S; Lee SO
[Ad] Endereço:Department of Food Science and Technology, Keimyung University, Daegu 42601, Republic of Korea.
[Ti] Título:Inactivation of the orphan nuclear receptor NR4A1 contributes to apoptosis induction by fangchinoline in pancreatic cancer cells.
[So] Source:Toxicol Appl Pharmacol;332:32-39, 2017 Oct 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous studies have demonstrated that the orphan nuclear receptor NR4A1 is overexpressed in human pancreatic cancer and antagonizing this receptor promotes apoptosis and inhibits pancreatic cancer cells and tumor growth. In the present study, we identified fangchinoline, a bisbenzyltetrahydroisoquinoline alkaloid from Stephania tetrandra, as a new inactivator of nuclear NR4A1 and demonstrated that fangchinoline inhibits cell proliferation and induces apoptosis, in part, via the NR4A1-dependent pro-apoptotic pathways in human pancreatic cancer cells. It decreased expression of the antiapoptotic protein survivin by inhibiting Sp1-mediated transcription and induced oxidative stress-mediated endoplasmic reticulum (ER) stress in pancreatic cancer cells. These results suggest that inhibition of NR4A1-mediated transcriptional activity was involved in the anticancer effects of fangchinoline, and fangchinoline represents a novel class of mechanism-based anticancer agents targeting NR4A1 that is overexpressed in pancreatic cancer.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Benzilisoquinolinas/farmacologia
Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Neoplasias Pancreáticas/patologia
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Seres Humanos
Proteínas Inibidoras de Apoptose/genética
Proteínas Inibidoras de Apoptose/metabolismo
Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Estresse Oxidativo/efeitos dos fármacos
Neoplasias Pancreáticas/tratamento farmacológico
Espécies Reativas de Oxigênio/metabolismo
Fator de Transcrição Sp1/antagonistas & inibidores
Fator de Transcrição Sp1/genética
Fator de Transcrição Sp1/metabolismo
Stephania tetrandra/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (BIRC5 protein, human); 0 (Benzylisoquinolines); 0 (Inhibitor of Apoptosis Proteins); 0 (NR4A1 protein, human); 0 (Nuclear Receptor Subfamily 4, Group A, Member 1); 0 (Reactive Oxygen Species); 0 (Sp1 Transcription Factor); 0 (Sp1 protein, human); 953592C3ZB (fangchinoline)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170730
[St] Status:MEDLINE


  7 / 1517 MEDLINE  
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[PMID]:28697340
[Au] Autor:Gu Y; Zhang J; Ma X; Kim BW; Wang H; Li J; Pan Y; Xu Y; Ding L; Yang L; Guo C; Wu X; Wu J; Wu K; Gan X; Li G; Li L; Forman SJ; Chan WC; Xu R; Huang W
[Ad] Endereço:Molecular and Cellular Biology of Cancer Program & Department of Diabetes Complications and Metabolism, Beckman Research Institute, City of Hope, Duarte, CA 91010, USA.
[Ti] Título:Stabilization of the c-Myc Protein by CAMKIIγ Promotes T Cell Lymphoma.
[So] Source:Cancer Cell;32(1):115-128.e7, 2017 Jul 10.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although high c-Myc protein expression is observed alongside MYC amplification in some cancers, in most cases protein overexpression occurs in the absence of gene amplification, e.g., T cell lymphoma (TCL). Here, Ca /calmodulin-dependent protein kinase II γ (CAMKIIγ) was shown to stabilize the c-Myc protein by directly phosphorylating it at serine 62 (S62). Furthermore, CAMKIIγ was shown to be essential for tumor maintenance. Inhibition of CAMKIIγ with a specific inhibitor destabilized c-Myc and reduced tumor burden. Importantly, high CAMKIIγ levels in patient TCL specimens correlate with increased c-Myc and pS62-c-Myc levels. Together, the CAMKIIγ:c-Myc axis critically influences the development and maintenance of TCL and represents a potential therapeutic target for TCL.
[Mh] Termos MeSH primário: Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina/fisiologia
Linfoma de Células T/metabolismo
Proteínas Proto-Oncogênicas c-myc/fisiologia
[Mh] Termos MeSH secundário: Animais
Benzilisoquinolinas/farmacologia
Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina/antagonistas & inibidores
Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina/genética
Proliferação Celular
Deleção de Genes
Xenoenxertos/metabolismo
Seres Humanos
Linfoma de Células T/patologia
Camundongos
Modelos Moleculares
Fosforilação
Proteínas Proto-Oncogênicas c-myc/genética
Proteínas Proto-Oncogênicas c-myc/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzylisoquinolines); 0 (Proto-Oncogene Proteins c-myc); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2); V5KM4XJ0WM (berbamine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170812
[Lr] Data última revisão:
170812
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE


  8 / 1517 MEDLINE  
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[PMID]:28587219
[Au] Autor:He CY; Fu J; Shou JW; Zhao ZX; Ren L; Wang Y; Jiang JD
[Ti] Título:In Vitro Study of the Metabolic Characteristics of Eight Isoquinoline Alkaloids from Natural Plants in Rat Gut Microbiota.
[So] Source:Molecules;22(6), 2017 Jun 04.
[Is] ISSN:1420-3049
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Gut microbiota is populated with an immense number of microorganisms, which can be regulated by dietary components and drugs to markedly affect the nutritional and health status of the host. Eight medicinal isoquinoline alkaloids from natural plants were cultured anaerobically with rat gut microbiota and an LC/MS -IT-TOF technique was used to identify the resulting metabolites. Palmatine, tetrahydropalmatine, dauricine, and tetrandrine containing nitro-hexatomic isoquinoline rings could be easily transformed by the intestinal flora in vitro and a total of nine demethylated metabolites were detected. However, sinomenine, homoharringtonine, harringtonine, and galanthamine, which all contained benzazepine, could not undergo demethylation. Computer-assisted docking was used to analyze the binding between these compounds and sterol 14α-demethylase. The computational results demonstrated that hydrophobic interactions were the main driving force for binding, but the steric hindrance produced by the benzazepine structure resulted in a weak interaction between the hit compounds and the enzyme. This work illustrated that gut microbiota were important in the metabolism of isoquinoline alkaloids.
[Mh] Termos MeSH primário: Alcaloides/metabolismo
Microbioma Gastrointestinal/fisiologia
Isoquinolinas/metabolismo
[Mh] Termos MeSH secundário: Alcaloides/química
Animais
Benzilisoquinolinas/química
Isoquinolinas/química
Masculino
Metabolômica
Simulação de Acoplamento Molecular
Ratos
Ratos Sprague-Dawley
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkaloids); 0 (Benzylisoquinolines); 0 (Isoquinolines); 29EX23D5AJ (tetrandrine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170619
[Lr] Data última revisão:
170619
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE


  9 / 1517 MEDLINE  
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[PMID]:28393701
[Au] Autor:Nawrot R
[Ad] Endereço:Department of Molecular Virology, Faculty of Biology, Adam Mickiewicz University in Poznan, Poznan. Poland.
[Ti] Título:Defense-related Proteins from Chelidonium majus L. as Important Components of its Latex.
[So] Source:Curr Protein Pept Sci;18(8):864-880, 2017.
[Is] ISSN:1875-5550
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The aim of this review is to cover most recent research on plant pathogenesis- and defenserelated proteins from latex-bearing medicinal plant Chelidonium majus (Papaveraceae) in the context of its importance for latex activity, function, pharmacological activities, and antiviral medicinal use. These results are compared with other latex-bearing plant species and recent research on proteins and chemical compounds contained in their latex. This is the first review, which clearly summarizes pathogenesisrelated (PR) protein families in latex-bearing plants pointing into their possible functions. The possible antiviral function of the latex by naming the abundant proteins present therein is also emphasized. Finally latex-borne defense system is hypothesized to constitute a novel type of preformed immediate defense response against viral, but also non-viral pathogens, and herbivores.
[Mh] Termos MeSH primário: Antivirais/química
Chelidonium/química
Látex/química
Proteínas de Plantas/química
[Mh] Termos MeSH secundário: Alcaloides/química
Alcaloides/isolamento & purificação
Alcaloides/farmacologia
Antivirais/isolamento & purificação
Antivirais/farmacologia
Benzilisoquinolinas/química
Benzilisoquinolinas/isolamento & purificação
Benzilisoquinolinas/farmacologia
Catecol Oxidase/química
Catecol Oxidase/isolamento & purificação
Catecol Oxidase/farmacologia
Quitinases/química
Quitinases/isolamento & purificação
Quitinases/farmacologia
Endopeptidases/química
Endopeptidases/isolamento & purificação
Endopeptidases/farmacologia
Lipoxigenase/química
Lipoxigenase/isolamento & purificação
Lipoxigenase/farmacologia
Peroxidases/química
Peroxidases/isolamento & purificação
Peroxidases/farmacologia
Proteínas de Plantas/isolamento & purificação
Proteínas de Plantas/farmacologia
Ribonucleases/química
Ribonucleases/isolamento & purificação
Ribonucleases/farmacologia
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Alkaloids); 0 (Antiviral Agents); 0 (Benzylisoquinolines); 0 (Latex); 0 (Plant Proteins); 53850-34-3 (thaumatin protein, plant); EC 1.10.3.1 (Catechol Oxidase); EC 1.11.1.- (Peroxidases); EC 1.13.11.12 (Lipoxygenase); EC 3.1.- (Ribonucleases); EC 3.2.1.14 (Chitinases); EC 3.4.- (Endopeptidases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.2174/1389203718666170406124013


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[PMID]:28393256
[Au] Autor:Tian DD; Zhang RX; Wu N; Yuan W; Luo SH; Chen HQ; Liu Y; Wang Y; He BC; Deng ZL
[Ad] Endereço:Department of Orthopaedics, The Second Affiliated Hospital, Chongqing Medical University, Yuzhong, Chongqing 400010, P.R. China.
[Ti] Título:Tetrandrine inhibits the proliferation of human osteosarcoma cells by upregulating the PTEN pathway.
[So] Source:Oncol Rep;37(5):2795-2802, 2017 May.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Tetrandrine (TET) is a natural product isolated from the Chinese herb Stephania tetrandra S. Moore and has been reported to have antiproliferation and apoptosis-inducing activity in various malignant tumor cells. However, the exact molecular mechanisms underlying these effects remain unclear. In the present study, we tested the antiproliferation effect of TET on osteosarcoma (OS) 143B cells and explored the possible potential molecular mechanism in this process. Using CCK-8 assay and flow cytometry, we found that TET inhibited proliferation, induced apoptosis and arrested the cell cycle of the 143B cells. Using a xenograft tumor model of human OS, tetrandrine was found to inhibit tumor growth in vivo. TET increased the protein level of phosphatase and tensin homolog (PTEN) and decreased its phosphorylation as detected by western blot analysis and immunohistochemistry.Overexpression of PTEN strengthened the anticancer effect of TET, while knockdown of PTEN attenuated it. Meanwhile, TET activated p38 MAPK and increased its phosphorylation. Our findings suggest that TET may be a potential anticancer drug for OS. In addition, its effects may be mediated by the upregulation of PTEN. Moreover the expression alteration of PTEN and p-PTEN was mediated by the TET-induced activation of p38 MAPK in a direct or indirect manner.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/administração & dosagem
Benzilisoquinolinas/administração & dosagem
Neoplasias Ósseas/tratamento farmacológico
Osteossarcoma/tratamento farmacológico
PTEN Fosfo-Hidrolase/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Animais
Antineoplásicos Fitogênicos/farmacologia
Benzilisoquinolinas/farmacologia
Neoplasias Ósseas/metabolismo
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Camundongos
Osteossarcoma/metabolismo
Transdução de Sinais/efeitos dos fármacos
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Benzylisoquinolines); 29EX23D5AJ (tetrandrine); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (PTEN protein, human)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170627
[Lr] Data última revisão:
170627
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.3892/or.2017.5560



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