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[PMID]:28449948
[Au] Autor:Lutz SZ; Ullrich A; Häring HU; Ullrich S; Gerst F
[Ad] Endereço:German Center for Diabetes Research (DZD e.V.), Germany; Institute for Diabetes Research and Metabolic Diseases IDM of the Helmholtz Center Munich at the Eberhard-Karls-University of Tübingen, Germany; University Hospital Tübingen, Internal Medicine IV, Endocrinology, Diabetology, Angiology, Nephrol
[Ti] Título:Sunitinib specifically augments glucose-induced insulin secretion.
[So] Source:Cell Signal;36:91-97, 2017 Aug.
[Is] ISSN:1873-3913
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The tyrosine kinase inhibitor sunitinib is used for the treatment of numerous cancers in humans. In diabetic patients, sunitinib lowers blood glucose levels and improves glycaemic control. This study aims to analyse whether sunitinib has specific and direct effects on insulin secreting ß-cells. Regulation of insulin secretion, of cellular cAMP levels and activation of signalling pathways were examined upon exposure of rat insulinoma INS-1E cells to sunitinib under specific stimulatory and inhibitory conditions. Secreted insulin and cellular cAMP levels were measured using RIA and ELISA, respectively. Protein phosphorylations were examined on western blots. Sunitinib enhanced glucose-induced insulin secretion (GIIS) concentration-dependently, reaching a maximal stimulation at 2µM. Sunitinib further augmented insulin secretion in the presence of elevated cAMP levels and the FFAR1 agonists. Adrenaline and the PKA inhibitor H89 counteracted the stimulatory effect of sunitinib on secretion. However, sunitinib altered neither the cellular levels of cAMP nor the phosphorylation of PKA. Sunitinib did not reduce IGF-1-induced phosphorylation of AKT/PKB and ERK1/2. In conclusion, these results suggest that sunitinib stimulates GIIS by a direct effect on ß-cells, which may contribute to the glucose-lowering action of the tyrosine kinase inhibitor in humans.
[Mh] Termos MeSH primário: Glucose/farmacologia
Indóis/farmacologia
Insulina/secreção
Pirróis/farmacologia
[Mh] Termos MeSH secundário: Compostos de Anilina
Animais
Linhagem Celular
Colforsina/farmacologia
AMP Cíclico/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/antagonistas & inibidores
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Fator de Crescimento Insulin-Like I/metabolismo
Isoquinolinas/farmacologia
Fenilpropionatos
Fosforilação/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
Ratos
Transdução de Sinais/efeitos dos fármacos
Sulfonamidas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (H-89 dihydrochloride hydrate); 0 (Indoles); 0 (Insulin); 0 (Isoquinolines); 0 (Phenylpropionates); 0 (Protein Kinase Inhibitors); 0 (Pyrroles); 0 (Sulfonamides); 0 (TUG-469); 1F7A44V6OU (Colforsin); 67763-96-6 (Insulin-Like Growth Factor I); E0399OZS9N (Cyclic AMP); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); IY9XDZ35W2 (Glucose); V99T50803M (sunitinib)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


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[PMID]:29386430
[Au] Autor:Hanawa T; Kawano Y; Satoh M
[Ad] Endereço:Faculty of Pharmaceutical Sciences, Tokyo University of Science.
[Ti] Título:[Development of "Patient Friendly Formulations" to Counter the Side Effects of Cancer Chemotherapy].
[So] Source:Yakugaku Zasshi;138(2):169-175, 2018.
[Is] ISSN:1347-5231
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo: Anticancer drug-induced stomatitis develops in 30% to 40% of cancer patients undergoing chemotherapy. However, medications for this condition are not commercially available in Japan. The "hospital formulation" is a customized medicine which hospital pharmacists prepare when doctors cannot carry out the medical therapy most suitable for a patient using commercial medicines. However, as the duties of pharmacists increase, use of the "hospital fomulation" decreases. Therefore, development of "hospital fomulations" based on individual evidence has a limit. Irsogladine maleate (IM) is a drug with gastric mucosal protective properties. IM increases intracellular cAMP levels in the gastric mucosa and activates communication between cells. It has been reported that the oral administration of IM reduces the incidence of 5-FU-based chemotherapy-induced stomatitis. However, there have been no reports on the effect of the direct use of IM in treating stomatitis. Therefore, we studied the development of an IM oral spray for stomatitis treatment, and obtained evidence of a direct effect in an animal experiment using a stomatitis model. Next, rebamipide mouthwash was administered to patients who had stomatitis caused by cancer chemotherapy. The total scores were classified into Grades 0 to 4 and evaluated as a stomatitis evaluation score (SES). When comparing SES and changes in the stomatitis area in patients, gradual reductions in the extent of stomatitis were observed, even during the period when SES did not change. Having patients fill in an observation chart was effective for grasping changes in symptoms in outpatients.
[Mh] Termos MeSH primário: Alanina/análogos & derivados
Antineoplásicos/efeitos adversos
Composição de Medicamentos
Quinolonas/administração & dosagem
Estomatite/induzido quimicamente
Estomatite/tratamento farmacológico
Triazinas/administração & dosagem
Triazinas/farmacologia
[Mh] Termos MeSH secundário: Administração Oral
Alanina/administração & dosagem
Animais
Comunicação Celular/efeitos dos fármacos
AMP Cíclico/metabolismo
Modelos Animais de Doenças
Medicina Baseada em Evidências
Mucosa Gástrica/citologia
Mucosa Gástrica/metabolismo
Seres Humanos
Antissépticos Bucais
Estomatite/prevenção & controle
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Mouthwashes); 0 (Quinolones); 0 (Triazines); E0399OZS9N (Cyclic AMP); LR583V32ZR (rebamipide); OF5P57N2ZX (Alanine); QBX79NZC1D (irsogladine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180202
[St] Status:MEDLINE
[do] DOI:10.1248/yakushi.17-00174-2


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[PMID]:29262712
[Au] Autor:Mbovane MS; Gangireddygari VSR; Nyoni H; Ntushelo K
[Ad] Endereço:1 Department of Agriculture and Animal Health, University of South Africa , Florida, 1710 South Africa.
[Ti] Título:Acetaldehyde suppresses growth, changes conidia morphology and reduces the production of adenosine 3',5'-cyclic monophosphate in a dose dependent manner in Alternaria alternata.
[So] Source:Acta Biol Hung;68(4):490-492, 2017 Dec.
[Is] ISSN:0236-5383
[Cp] País de publicação:Hungary
[La] Idioma:eng
[Ab] Resumo:One-day-old cultures of the plant pathogenic fungus Alternaria alternata were exposed to 0%, 5% and 10% acetaldehyde mixed with distilled water. Fungal growth data showed that, overall, the 5% and the 10% acetaldehyde treatments significantly inhibited the growth of A. alternata, and that acetyldehyde also facilitated maturity and multicellularity of fungal conidia. The increase of the acetyldehyde dose also caused correlated decrease of adenosine 3',5'-cyclic monophosphate produced by A. alternata.
[Mh] Termos MeSH primário: Acetaldeído/farmacologia
Alternaria/fisiologia
AMP Cíclico/metabolismo
Esporos Fúngicos/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Alternaria/citologia
Relação Dose-Resposta a Droga
Esporos Fúngicos/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
E0399OZS9N (Cyclic AMP); GO1N1ZPR3B (Acetaldehyde)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE
[do] DOI:10.1556/018.68.2017.4.13


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[PMID]:29198864
[Au] Autor:Jiao GS; Kim S; Moayeri M; Thai A; Cregar-Hernandez L; McKasson L; O'Malley S; Leppla SH; Johnson AT
[Ad] Endereço:Hawaii Biotech, 650 Iwilei Road, Suite 204, Honolulu, HI 96817, USA.
[Ti] Título:Small molecule inhibitors of anthrax edema factor.
[So] Source:Bioorg Med Chem Lett;28(2):134-139, 2018 01 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Anthrax is a highly lethal disease caused by the Gram-(+) bacteria Bacillus anthracis. Edema toxin (ET) is a major contributor to the pathogenesis of disease in humans exposed to B. anthracis. ET is a bipartite toxin composed of two proteins secreted by the vegetative bacteria, edema factor (EF) and protective antigen (PA). Our work towards identifying a small molecule inhibitor of anthrax edema factor is the subject of this letter. First we demonstrate that the small molecule probe 5'-Fluorosulfonylbenzoyl 5'-adenosine (FSBA) reacts irreversibly with EF and blocks enzymatic activity. We then show that the adenosine portion of FSBA can be replaced to provide more drug-like molecules which are up to 1000-fold more potent against EF relative to FSBA, display low cross reactivity when tested against a panel of kinases, and are nanomolar inhibitors of EF in a cell-based assay of cAMP production.
[Mh] Termos MeSH primário: Antraz/tratamento farmacológico
Bacillus anthracis/efeitos dos fármacos
Toxinas Bacterianas/antagonistas & inibidores
Bibliotecas de Moléculas Pequenas/farmacologia
[Mh] Termos MeSH secundário: Animais
Antígenos de Bactérias/farmacologia
Toxinas Bacterianas/farmacologia
AMP Cíclico/antagonistas & inibidores
AMP Cíclico/biossíntese
Relação Dose-Resposta a Droga
Seres Humanos
Camundongos
Estrutura Molecular
Proteínas Quinases/metabolismo
Células RAW 264.7
Bibliotecas de Moléculas Pequenas/síntese química
Bibliotecas de Moléculas Pequenas/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Bacterial Toxins); 0 (Small Molecule Libraries); 0 (anthrax toxin); E0399OZS9N (Cyclic AMP); EC 2.7.- (Protein Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


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[PMID]:29183759
[Au] Autor:Kim HJ; Lee E; Lee M; Ahn S; Kim J; Liu J; Jin SH; Ha J; Bae IH; Lee TR; Noh M
[Ad] Endereço:Basic Research and Innovation Division, AmorePacific Corporation R&D Center, Yongin, Gyeounggi-do 17074, Republic of Korea.
[Ti] Título:Phosphodiesterase 4B plays a role in benzophenone-3-induced phototoxicity in normal human keratinocytes.
[So] Source:Toxicol Appl Pharmacol;338:174-181, 2018 01 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Benzophenone-3 (BP-3), which is extensively used in organic sunscreen, has phototoxic potential in human skin. Phosphodiesterase 4B (PDE4B) has a well-established role in inflammatory responses in immune cells. Currently, it is unknown if PDE4B is associated with BP-3-induced phototoxicity in normal human keratinocytes (NHKs). We found that BP-3 significantly increased PDE4B expression in ultraviolet B (UVB)-irradiated NHKs. Notably, BP-8, a sunscreen agent that shares the 2-hydroxy-4-methoxyphenyl methanone moiety with BP-3, also upregulated PDE4B expression in NHKs. Upon UVB irradiation, BP-3 upregulated the expression of pro-inflammatory factors, such as prostaglandin endoperoxide synthase 2, tumor necrosis factor α, interleukin 8, and S100A7, and downregulated the level of cornified envelope associated proteins, which are important in the development of the epidermal permeability barrier. The additive effects of UVB-activated BP-3 on the expression of both pro-inflammatory mediators and cornified envelope associated proteins were antagonized by treatment with the PDE4 inhibitor rolipram. The BP-3 and UVB co-stimulation-induced PDE4B upregulation and its association with the upregulation of pro-inflammatory mediators and the downregulation of epidermal differentiation markers were confirmed in a reconstituted three dimensional human epidermis model. Therefore, PDE4B has a role in the mechanism of BP-3-induced phototoxicity.
[Mh] Termos MeSH primário: Benzofenonas/toxicidade
Nucleotídeo Cíclico Fosfodiesterase do Tipo 4/fisiologia
Dermatite Fototóxica/etiologia
Queratinócitos/efeitos dos fármacos
[Mh] Termos MeSH secundário: AMP Cíclico/fisiologia
Nucleotídeo Cíclico Fosfodiesterase do Tipo 4/genética
Dinoprostona/biossíntese
Seres Humanos
Interleucina-8/biossíntese
Fator de Necrose Tumoral alfa/biossíntese
Raios Ultravioleta
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Benzophenones); 0 (Interleukin-8); 0 (Tumor Necrosis Factor-alpha); 95OOS7VE0Y (oxybenzone); E0399OZS9N (Cyclic AMP); EC 3.1.4.17 (Cyclic Nucleotide Phosphodiesterases, Type 4); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE


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[PMID]:28458351
[Au] Autor:Yamaguchi M; Saito SY; Nishiyama R; Nakamura M; Todoroki K; Toyo'oka T; Ishikawa T
[Ad] Endereço:Department of Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka.
[Ti] Título:Caffeine Suppresses the Activation of Hepatic Stellate Cells cAMP-Independently by Antagonizing Adenosine Receptors.
[So] Source:Biol Pharm Bull;40(5):658-664, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:During liver injury, hepatic stellate cells (HSCs) are activated by various cytokines and transdifferentiated into myofibroblast-like activated HSCs, which produce collagen, a major source of liver fibrosis. Therefore, the suppression of HSC activation is regarded as a therapeutic target for liver fibrosis. Several epidemiological reports have revealed that caffeine intake decreases the risk of liver disease. In this study, therefore, we investigated the effect of caffeine on the activation of primary HSCs isolated from mice. Caffeine suppressed the activation of HSC in a concentration-dependent manner. BAPTA-AM, an intracellular Ca chelator, had no effect on the caffeine-induced suppression of HSC activation. None of the isoform-selective inhibitors of phosphodiesterase1 to 5 affected changes in the morphology of HSC during activation, whereas CGS-15943, an adenosine receptor antagonist, inhibited them. Caffeine had no effect on intracellular cAMP level or on the phosphorylation of extracellular signal-regulated kinase (ERK)1/2. In contrast, caffeine significantly decreased the phosphorylation of Akt1. These results suggest that caffeine inhibits HSC activation by antagonizing adenosine receptors, leading to Akt1 signaling activation.
[Mh] Termos MeSH primário: Cafeína/farmacologia
AMP Cíclico/metabolismo
Células Estreladas do Fígado/efeitos dos fármacos
Inibidores de Fosfodiesterase/farmacologia
Receptores Purinérgicos P1/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Quelantes/farmacologia
Relação Dose-Resposta a Droga
Ácido Egtázico/análogos & derivados
Ácido Egtázico/farmacologia
Cirrose Hepática/tratamento farmacológico
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Masculino
Camundongos
Fosforilação
Quinazolinas/farmacologia
Triazóis/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chelating Agents); 0 (Phosphodiesterase Inhibitors); 0 (Quinazolines); 0 (Receptors, Purinergic P1); 0 (Triazoles); 104615-18-1 (9-chloro-2-(2-furyl)-(1,2,4)triazolo(1,5-c)quinazolin-5-imine); 139890-68-9 (1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester); 3G6A5W338E (Caffeine); 526U7A2651 (Egtazic Acid); E0399OZS9N (Cyclic AMP)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00947


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[PMID]:28463107
[Au] Autor:Monterisi S; Lobo MJ; Livie C; Castle JC; Weinberger M; Baillie G; Surdo NC; Musheshe N; Stangherlin A; Gottlieb E; Maizels R; Bortolozzi M; Micaroni M; Zaccolo M
[Ad] Endereço:Department of Physiology Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
[Ti] Título:PDE2A2 regulates mitochondria morphology and apoptotic cell death via local modulation of cAMP/PKA signalling.
[So] Source:Elife;6, 2017 05 02.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:cAMP/PKA signalling is compartmentalised with tight spatial and temporal control of signal propagation underpinning specificity of response. The cAMP-degrading enzymes, phosphodiesterases (PDEs), localise to specific subcellular domains within which they control local cAMP levels and are key regulators of signal compartmentalisation. Several components of the cAMP/PKA cascade are located to different mitochondrial sub-compartments, suggesting the presence of multiple cAMP/PKA signalling domains within the organelle. The function and regulation of these domains remain largely unknown. Here, we describe a novel cAMP/PKA signalling domain localised at mitochondrial membranes and regulated by PDE2A2. Using pharmacological and genetic approaches combined with real-time FRET imaging and high resolution microscopy, we demonstrate that in rat cardiac myocytes and other cell types mitochondrial PDE2A2 regulates local cAMP levels and PKA-dependent phosphorylation of Drp1. We further demonstrate that inhibition of PDE2A, by enhancing the hormone-dependent cAMP response locally, affects mitochondria dynamics and protects from apoptotic cell death.
[Mh] Termos MeSH primário: Apoptose
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
AMP Cíclico/metabolismo
Nucleotídeo Cíclico Fosfodiesterase do Tipo 2/metabolismo
Dinaminas/metabolismo
Mitocôndrias/metabolismo
Mitocôndrias/ultraestrutura
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Seres Humanos
Camundongos
Fosforilação
Processamento de Proteína Pós-Traducional
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
E0399OZS9N (Cyclic AMP); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 3.1.4.17 (Cyclic Nucleotide Phosphodiesterases, Type 2); EC 3.1.4.17 (Pde2a protein, rat); EC 3.6.5.5 (Drp1 protein, rat); EC 3.6.5.5 (Dynamins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180211
[Lr] Data última revisão:
180211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:29317250
[Au] Autor:Park SH; Cho JY; Oh SW; Kang M; Lee SE; Yoo JA; Jung K; Lee J; Lee SY; Lee J
[Ad] Endereço:Department of Bio and Chemical Engineering, Hongik University, 300-16 Sejong City, Republic of Korea.
[Ti] Título:Arctigenin protects against ultraviolet-A-induced damage to stemness through inhibition of the NF-κB/MAPK pathway.
[So] Source:Chem Biol Interact;282:63-68, 2018 Feb 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The stemness of stem cells is negatively affected by ultraviolet A (UVA) irradiation. This study was performed to examine the effects of arctigenin on UVA-irradiation-induced damage to the stemness of human mesenchymal stem cells (hMSCs) derived from adipose tissue. The mechanisms of action of arctigenin were also investigated. A BrdU-incorporation assay demonstrated that arctigenin attenuated the UVA-induced reduction of the cellular proliferative potential. Arctigenin also increased the UVA-induced reduction in stemness of hMSCs by upregulating stemness-related genes such as SOX2, OCT4, and NANOG. In addition, the UVA-induced reduction in the mRNA expression level of hypoxia-inducible factor (HIF)-1α was significantly recovered by arctigenin. The antagonizing effect of arctigenin on UVA irradiation was mediated by reduced PGE production through the inhibition of MAPKs (p42/44 MAPK, p38 MAPK, and JNK) and NF-κB. Overall, these findings suggest that arctigenin can ameliorate the reduced stemness of hMSCs induced by UVA irradiation. The effects of arctigenin are mediated by PGE -cAMP signaling-dependent upregulation of HIF-1α. Therefore, arctigenin could be used as an antagonist to attenuate the effects of UVA irradiation.
[Mh] Termos MeSH primário: Furanos/farmacologia
Lignanas/farmacologia
Células Mesenquimais Estromais/efeitos dos fármacos
Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
Substâncias Protetoras/farmacologia
Transdução de Sinais/efeitos dos fármacos
Raios Ultravioleta/efeitos adversos
[Mh] Termos MeSH secundário: Proliferação Celular/efeitos dos fármacos
Células Cultivadas
AMP Cíclico/metabolismo
Dinoprostona/metabolismo
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Células Mesenquimais Estromais/metabolismo
Proteína Homeobox Nanog/metabolismo
Fator 3 de Transcrição de Octâmero/metabolismo
RNA Mensageiro/metabolismo
Fatores de Transcrição SOXB1/metabolismo
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Furans); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Lignans); 0 (NF-kappa B); 0 (Nanog Homeobox Protein); 0 (Octamer Transcription Factor-3); 0 (Protective Agents); 0 (RNA, Messenger); 0 (SOXB1 Transcription Factors); E0399OZS9N (Cyclic AMP); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); K7Q1JQR04M (Dinoprostone); U76MR9VS6M (arctigenin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE


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[PMID]:29225111
[Au] Autor:Xu X; Chen J; Hu L; Liang M; Wang X; Feng S; Shen J; Luan X
[Ad] Endereço:Department of Endocrinology, the First People's Hospital of Foshan, Foshan, Guangdong 52800, China; Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Endocrinology, the Third Affiliated Hospital of Southern Medical University, Guangzhou, Guangdong 510515, China.
[Ti] Título:Liraglutide regulates the viability of pancreatic α-cells and pancreatic ß-cells through cAMP-PKA signal pathway.
[So] Source:Life Sci;195:87-94, 2018 Feb 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: As a glucagon-like peptide-1 receptor agonist, liraglutide could effectively increase insulin secretion from pancreatic ß-cells and suppress glucagon secretion from pancreatic α-cells in the treatment of hyperglycemia in type 2 diabetes patients. However, the mechanisms for the different regulation of pancreatic α-cells and ß-cells are still unclear. In this study, we mainly explored the different effects of liraglutide on mouse pancreatic α-cell line and ß-cell line in vitro. MAIN METHODS: Herein, mouse pancreatic α-cell line, α-TC1-6, and mouse pancreatic ß-cell line, ß-TC-tet, were used to analyze the biological effects of liraglutide in different concentrations. Cell proliferation, cell apoptosis and cell secretion ability were detected in different groups. Besides, the level of miR-375 and cAMP-PKA signal pathway were further evaluated using qPCR and western blot. KEY FINDINGS: The results indicated that liraglutide could increase the level of miR-375 and cell apoptosis in pancreatic α-cells through inhibiting the cAMP-PKA signal pathway, but activate cAMP-PKA signal pathway in pancreatic ß-cells, and further lead to the down-regulation of miR-375 and improve cell viability. Therefore, the treatment with liraglutide could down-regulate the glucagon secretion ability of α-TC1-6 cells, and the insulin secretion ability of ß-TC-tet cells was enhanced with the liraglutide treatment in a dose-dependent manner. SIGNIFICANCE: In conclusion, we mainly found that liraglutide could regulate the viability of pancreatic α-cells and pancreatic ß-cells through inhibiting and activating cAMP-PKA signal pathway respectively. The better understanding of the mechanism could help us to develop more novel therapy methods for diabetes in the future.
[Mh] Termos MeSH primário: Proteínas Quinases Dependentes de AMP Cíclico/fisiologia
AMP Cíclico/fisiologia
Células Secretoras de Glucagon/efeitos dos fármacos
Hipoglicemiantes/farmacologia
Células Secretoras de Insulina/efeitos dos fármacos
Liraglutida/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Glucagon/secreção
Células Secretoras de Glucagon/secreção
Insulina/secreção
Células Secretoras de Insulina/secreção
Camundongos
MicroRNAs/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypoglycemic Agents); 0 (Insulin); 0 (MicroRNAs); 0 (Mirn375 microRNA, mouse); 839I73S42A (Liraglutide); 9007-92-5 (Glucagon); E0399OZS9N (Cyclic AMP); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE


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[PMID]:28448438
[Au] Autor:Khamrang T; Hung KC; Hsia CH; Hsieh CY; Velusamy M; Jayakumar T; Sheu JR
[Ad] Endereço:Department of Chemistry, North Eastern Hill University, Shillong 793022, India. themmilakhamrang@gmail.com.
[Ti] Título:Antiplatelet Activity of a Newly Synthesized Novel Ruthenium (II): A Potential Role for Akt/JNK Signaling.
[So] Source:Int J Mol Sci;18(5), 2017 Apr 27.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:In oncotherapy, ruthenium complexes are considered as potential alternatives for platinum compounds, and have been proved as promising anticancer drugs with high efficacy and lesser side effects. Platelet activation plays a major role in cancer metastasis and progression. Hence, this study explored the effect of a newly synthesized ruthenium complex, [Ru(η6-cymene)(L)Cl]BF4(TQ5), where L = 4-phenyl-2-pyridin-2-yl-quinazoline), on human platelet activation. TQ5 (3-5 µM) inhibited concentration-dependent collagen-induced platelet aggregation in washed human platelets. However, this compound only inhibited platelet aggregation at a maximum concentration of 500 and 100 µM against thrombin and 9,11-dideoxy-11α, 9α-epoxymethanoprostaglandin (U46619)-induced stimulation, respectively. TQ5 inhibited collagen-induced ATP release and calcium mobilization ([Ca ] ), without inducing cell cytotoxicity. In addition, neither SQ22536, an adenylate cyclase inhibitor, nor 1H-[1,2,4] oxadiazolo [4,3-a]quinoxalin-1-one (ODQ), a guanylate cyclase inhibitor, significantly reversed the TQ5-mediated inhibition of platelet aggregation. TQ5 inhibited the collagen-induced phosphorylation of protein kinase B (Akt) and c-Jun N-terminal kinase (JNK), but did not effectively inhibit extracellular signal-regulated kinase 1/2 (ERK1/2) and p38-mitogen-activated protein kinase (p38-MAPK) in human platelets. Additionally, TQ5 significantly prolonged the closure time in whole blood and increased the occlusion time of thrombotic platelet plug formation in mice. This study demonstrates, for the first time, that a newly synthesized ruthenium complex, TQ5, exhibits potent antiplatelet activity by hindering ATP release and [Ca ] , and by decreasing the activation of Akt/JNK signals. Together, these results suggest that TQ5 could be developed as a therapeutic agent that helps prevent or treat thromboembolic disorders, since it is found to be potently more effective than a well-established antithrombotic aspirin.
[Mh] Termos MeSH primário: Plaquetas/efeitos dos fármacos
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Agregação Plaquetária/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Rutênio/química
Rutênio/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Ácido 15-Hidroxi-11 alfa,9 alfa-(epoximetano)prosta-5,13-dienoico/farmacologia
Trifosfato de Adenosina/metabolismo
Plaquetas/citologia
Plaquetas/metabolismo
Cálcio/metabolismo
Colágeno/farmacologia
Complexos de Coordenação/síntese química
Complexos de Coordenação/farmacologia
AMP Cíclico/metabolismo
Seres Humanos
Oxidiazóis/farmacologia
Fosforilação/efeitos dos fármacos
Ativação Plaquetária/efeitos dos fármacos
Inibidores da Agregação de Plaquetas/síntese química
Inibidores da Agregação de Plaquetas/farmacologia
Quinoxalinas/farmacologia
Trombina/farmacologia
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one); 0 (Coordination Complexes); 0 (Oxadiazoles); 0 (Platelet Aggregation Inhibitors); 0 (Quinoxalines); 76898-47-0 (15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid); 7UI0TKC3U5 (Ruthenium); 8L70Q75FXE (Adenosine Triphosphate); 9007-34-5 (Collagen); E0399OZS9N (Cyclic AMP); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 3.4.21.5 (Thrombin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE



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