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  1 / 10839 MEDLINE  
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[PMID]:29425766
[Au] Autor:Tahara A; Takasu T
[Ad] Endereço:Candidate Discovery Science Laboratories, Astellas Pharma Inc., Ibaraki, Japan. Electronic address: atsuo.tahara@jp.astellas.com.
[Ti] Título:Antidiabetic effects of SGLT2 inhibitor ipragliflozin in type 2 diabetic mice fed diets containing different carbohydrate contents.
[So] Source:Life Sci;197:80-90, 2018 Mar 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Daily intake of carbohydrates differs among individual patients with type 2 diabetes. Here, we investigated whether or not dietary carbohydrate content affects the efficacy of the sodium-glucose cotransporter 2 (SGLT2) inhibitor ipragliflozin in type 2 diabetic mice. MAIN METHODS: Diabetic mice were fed a regular (50% kcal), high (75% kcal)-, or low (25% kcal)-carbohydrate diet. Ipragliflozin was orally administered once a day for 4 weeks. KEY FINDINGS: In all groups, mice exhibited characteristics of type 2 diabetes, including hyperglycemia, hyperinsulinemia, and obesity. Hyperglycemia was more severe in the high-carbohydrate diet group and milder in the low-carbohydrate diet group than in the regular diet group. In all diabetic mice, ipragliflozin significantly increased urinary glucose excretion and improved hyperglycemia, hyperinsulinemia, glucose tolerance, insulin resistance, obesity, and nephropathy. Although these antidiabetic effects of ipragliflozin were more marked in the high-carbohydrate diet group (which showed more severe hyperglycemia) than in the other two groups, no significant differences in effective dose or degree of response were observed among the three groups. SIGNIFICANCE: The antidiabetic effects of ipragliflozin were not greatly affected by dietary carbohydrate content, suggesting that ipragliflozin may have similar efficacy for patients with type 2 diabetes regardless of carbohydrate intake.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/tratamento farmacológico
Diabetes Mellitus Tipo 2/tratamento farmacológico
Dieta
Carboidratos da Dieta/farmacologia
Glucosídeos/farmacologia
Hipoglicemiantes/farmacologia
Transportador 2 de Glucose-Sódio/antagonistas & inibidores
Tiofenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Diabetes Mellitus Tipo 2/sangue
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Dietary Carbohydrates); 0 (Glucosides); 0 (Hypoglycemic Agents); 0 (Slc5a2 protein, mouse); 0 (Sodium-Glucose Transporter 2); 0 (Thiophenes); 3N2N8OOR7X (ipragliflozin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180210
[St] Status:MEDLINE


  2 / 10839 MEDLINE  
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[PMID]:29409796
[Au] Autor:Li H; Shin SE; Seo MS; An JR; Choi IW; Jung WK; Firth AL; Lee DS; Yim MJ; Choi G; Lee JM; Na SH; Park WS
[Ad] Endereço:Institute of Medical Sciences, Department of Physiology, Kangwon National University School of Medicine, Chuncheon 24341, South Korea.
[Ti] Título:The anti-diabetic drug dapagliflozin induces vasodilation via activation of PKG and Kv channels.
[So] Source:Life Sci;197:46-55, 2018 Mar 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIM: Considering the clinical efficacy of dapagliflozin in patients with type 2 DM and the pathophysiological relevance of Kv channels for vascular reactivity. We investigate the vasodilatory effect of dapagliflozin and related mechanisms using phenylephrine (Phe)-induced contracted aortic rings. MATERIAL AND METHODS: Arterial tone measurement was performed in aortic smooth muscle. KEY FINDINGS: Application of dapagliflozin induced vasodilation in a concentration-dependent manner. Pre-treatment with the BK channel inhibitor paxilline, the K channel inhibitor glibenclamide, and the Kir channel inhibitor Ba did not change dapagliflozin-induced vasodilation. However, application of the Kv channels inhibitor 4-AP effectively inhibited dapagliflozin-induced vasodilation. Application of the Ca channel inhibitor nifedipine and the sarcoplasmic/endoplasmic reticulum Ca -ATPase (SERCA) pump inhibitor thapsigargin did not alter the vasodilatory effect of dapagliflozin. Moreover, the adenylyl cyclase inhibitor SQ 22536 and the protein kinase A (PKA) inhibitor KT 5720 had no effect on dapagliflozin-induced vasodilation. Although guanylyl cyclase inhibitors, NS 2028 and ODQ, did not reduce the vasodilatory effect of dapagliflozin, the protein kinase G (PKG) inhibitor KT 5823 effectively inhibited dapagliflozin-induced vasodilation. The vasodilatory effect of dapagliflozin was not affected by elimination of the endothelium. Furthermore, pretreatment with the nitric oxide synthase inhibitor L-NAME or the small-conductance Ca -activated K (SKCa) channel inhibitor apamin did not change the vasodilatory effect of dapagliflozin. SIGNIFICANCE: We concluded that dapagliflozin induced vasodilation via the activation of Kv channels and PKG, and was independent of other K channels, Ca channels, intracellular Ca , and the endothelium.
[Mh] Termos MeSH primário: Aorta/metabolismo
Compostos Benzidrílicos/farmacologia
Proteínas Quinases Dependentes de GMP Cíclico/metabolismo
Glucosídeos/farmacologia
Hipoglicemiantes/farmacologia
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
Canais de Potássio de Abertura Dependente da Tensão da Membrana/metabolismo
Vasodilatação/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Aorta/fisiopatologia
Ativação Enzimática/efeitos dos fármacos
Masculino
Músculo Liso Vascular/fisiopatologia
Coelhos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(3-(4-ethoxybenzyl)-4-chlorophenyl)-6-hydroxymethyltetrahydro-2H-pyran-3,4,5-triol); 0 (Benzhydryl Compounds); 0 (Glucosides); 0 (Hypoglycemic Agents); 0 (Potassium Channels, Voltage-Gated); EC 2.7.11.12 (Cyclic GMP-Dependent Protein Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180208
[St] Status:MEDLINE


  3 / 10839 MEDLINE  
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[PMID]:28480755
[Au] Autor:He Y; Wen L; Liu J; Li Y; Zheng F; Min W; Yue H; Pan P
[Ad] Endereço:a Department of Food Science and Engineering , Jilin Agricultural University , Changchun , China.
[Ti] Título:Optimisation of pulsed electric fields extraction of anthocyanin from Beibinghong Vitis Amurensis Rupr.
[So] Source:Nat Prod Res;32(1):23-29, 2018 Jan.
[Is] ISSN:1478-6427
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Beibinghong Vitis amurensis Rupr has wide plantation area, high productivity and rich anthocyanin. Common hot-extraction has poor deficiency and destroys anthocyanin severely. For Beibinghong V. amurensis Rupr as materials, response surface-optimised electric fields were used, the structure of Beibinghong was observed by SEM, antioxidant activity was measured by DPPH, ABTS and reducing force, the component of anthocyanin was analyzed by HPLC-MS. We found the content of total anthocyanin extracted by pulsed electric fields was 166.65 ± 3.88 mg/100 g.FW. Total anthocyanin from Beibinghong had high antioxidant activity, also contained multiple steady anthocyanin of delphinidin 3-O-glucoside, cyanidin 3-O-glucoside, petunidin 3-O-glucoside, peonidin 3-O-glucoside, malvidin 3-O-glucoside, delphinidin-3-O-(6-O-acetyl) glucoside and delphinidin-3-O-(6-O-p-coumaroyl) glucoside et al. In conclusion, the optimised pulsed electric fields method can quickly and efficiently extract several kinds of anthocyanins from V. amurensis Rupr. This study promoted the intensive processing of V. amurensis Rupr and widened the practical application of pulsed electric field technology.
[Mh] Termos MeSH primário: Antocianinas/isolamento & purificação
Fracionamento Químico/métodos
Vitis/química
[Mh] Termos MeSH secundário: Antocianinas/análise
Antocianinas/farmacologia
Antioxidantes/isolamento & purificação
Antioxidantes/farmacologia
Cromatografia Líquida de Alta Pressão/métodos
Estimulação Elétrica
Glucosídeos/análise
Espectrometria de Massas/métodos
Microscopia Eletrônica de Varredura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthocyanins); 0 (Antioxidants); 0 (Glucosides); 0 (delphinidin 3-O-glucopyranoside); 3419IIT8I0 (peonidin 3-glucoside); 6988-81-4 (petunidin-3-glucoside); 7084-24-4 (cyanidin 3-O-glucoside); 7228-78-6 (malvidin-3-glucoside)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE
[do] DOI:10.1080/14786419.2017.1324963


  4 / 10839 MEDLINE  
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[PMID]:27776917
[Au] Autor:Luconi M; Raimondi L; Di Franco A; Mannucci E
[Ad] Endereço:Endocrinology Unit, Dept. Clinical and Experimental Biomedical Sciences, University of Florence, Viale G. Pieraccini, 6, Florence, Italy.
[Ti] Título:Which is the main molecular target responsible for the cardiovascular benefits in the EMPA-REG OUTCOME trial? A journey through the kidney, the heart and other interesting places.
[So] Source:Nutr Metab Cardiovasc Dis;26(12):1071-1078, 2016 12.
[Is] ISSN:1590-3729
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The results of the EMPA-REG-OUTCOME trial on type 2 diabetic patients at high risk for prior cardiovascular events showed that empagliflozin produces a remarkable reduction in the rates of hospitalization for heart failure (35%), cardiovascular death (38%), and all-cause death (32%). This unexpected cardio-protective action cannot be accounted for by the improvement of "classical" cardiovascular risk factors. AIMS: This review aims at summarizing current knowledge on the cardiovascular action of SGLT2 inhibitors and discuss the different hypotheses formulated to explain the results of the EMPA-REG-OUTCOME-study. DATA SYNTHESIS: We discuss in detail the major cardiovascular outcomes of the study in the light of the potential systemic and myocardial mechanisms of action of the drug. In addition, we propose and speculate on a direct effect of empagliflozin on cardiomyocytes. CONCLUSIONS: The available evidence is insufficient to establish any of the proposed mechanisms of cardiovascular action of empagliflozin. While awaiting for the results of ongoing clinical studies with other SGLT2 inhibitors, the most promising putative mechanisms still deserve to be confirmed with specifically designed, yet unavailable, pre-clinical studies.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/uso terapêutico
Doenças Cardiovasculares/prevenção & controle
Diabetes Mellitus Tipo 2/tratamento farmacológico
Glucosídeos/uso terapêutico
Coração/fisiopatologia
Hipoglicemiantes/uso terapêutico
Rim/efeitos dos fármacos
Miócitos Cardíacos/efeitos dos fármacos
Transportador 2 de Glucose-Sódio/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Compostos Benzidrílicos/efeitos adversos
Doenças Cardiovasculares/mortalidade
Doenças Cardiovasculares/fisiopatologia
Ensaios Clínicos como Assunto
Diabetes Mellitus Tipo 2/sangue
Diabetes Mellitus Tipo 2/mortalidade
Diabetes Mellitus Tipo 2/fisiopatologia
Glucosídeos/efeitos adversos
Seres Humanos
Hipoglicemiantes/efeitos adversos
Rim/metabolismo
Rim/fisiopatologia
Miócitos Cardíacos/metabolismo
Medição de Risco
Fatores de Risco
Transportador 2 de Glucose-Sódio/metabolismo
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Glucosides); 0 (Hypoglycemic Agents); 0 (SLC5A2 protein, human); 0 (Sodium-Glucose Transporter 2); HDC1R2M35U (empagliflozin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  5 / 10839 MEDLINE  
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[PMID]:25868474
[Au] Autor:Maher S; Rasool S; Mehmood R; Perveen S; Tareen RB
[Ad] Endereço:a H. E. J. Research Institute of Chemistry, International Center for Chemical and Biological Sciences, University of Karachi , Karachi 75270 , Pakistan.
[Ti] Título:Trichosides A and B, new withanolide glucosides from Tricholepis eburnea.
[So] Source:Nat Prod Res;32(1):1-6, 2018 Jan.
[Is] ISSN:1478-6427
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Trichosides A (1) and B (2), new withanolide glucosides, have been isolated from the n-butanolic fraction of the 75% methanolic extract of aerial parts of Tricholepis eburnea. Their structures were elucidated through spectroscopic analysis including ESI-MS, 2D NMR and acid hydrolysis.
[Mh] Termos MeSH primário: Asteraceae/química
Glucosídeos/química
Vitanolídeos/química
[Mh] Termos MeSH secundário: Hidrólise
Espectroscopia de Ressonância Magnética
Estrutura Molecular
Espectrometria de Massas por Ionização por Electrospray
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucosides); 0 (Withanolides)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150415
[St] Status:MEDLINE
[do] DOI:10.1080/14786419.2015.1030340


  6 / 10839 MEDLINE  
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[PMID]:29360842
[Au] Autor:Liu F; Yang Y; Gao J; Ma C; Bi Y
[Ad] Endereço:College of Life Science, Shandong Normal University, Jinan, China.
[Ti] Título:A comparative transcriptome analysis of a wild purple potato and its red mutant provides insight into the mechanism of anthocyanin transformation.
[So] Source:PLoS One;13(1):e0191406, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, a red mutant was obtained through in vitro regeneration of a wild purple potato. High-performance liquid chromatography and Mass spectrometry analysis revealed that pelargonidin-3-O-glucoside and petunidin-3-O-glucoside were main anthocyanins in the mutant and wild type tubers, respectively. In order to thoroughly understand the mechanism of anthocyanin transformation in two materials, a comparative transcriptome analysis of the mutant and wild type was carried out through high-throughput RNA sequencing, and 295 differentially expressed genes (DEGs) were obtained. Real-time qRT-PCR validation of DEGs was consistent with the transcriptome date. The DEGs mainly influenced biological and metabolic pathways, including phenylpropanoid biosynthesis and translation, and biosynthesis of flavone and flavonol. In anthocyanin biosynthetic pathway, the analysis of structural genes expressions showed that three genes, one encoding phenylalanine ammonia-lyase, one encoding 4-coumarate-CoA ligase and one encoding flavonoid 3',5'-hydroxylasem were significantly down-regulated in the mutant; one gene encoding phenylalanine ammonia-lyase was significantly up-regulated. Moreover, the transcription factors, such as bZIP family, MYB family, LOB family, MADS family, zf-HD family and C2H2 family, were significantly regulated in anthocyanin transformation. Response proteins of hormone, such as gibberellin, abscisic acid and brassinosteroid, were also significantly regulated in anthocyanin transformation. The information contributes to discovering the candidate genes in anthocyanin transformation, which can serve as a comprehensive resource for molecular mechanism research of anthocyanin transformation in potatoes.
[Mh] Termos MeSH primário: Antocianinas/biossíntese
Antocianinas/genética
Solanum tuberosum/genética
Solanum tuberosum/metabolismo
[Mh] Termos MeSH secundário: Vias Biossintéticas/genética
Coenzima A Ligases/genética
Sistema Enzimático do Citocromo P-450/genética
Perfilação da Expressão Gênica
Regulação da Expressão Gênica de Plantas
Genes de Plantas
Glucosídeos/biossíntese
Glucosídeos/genética
Sequenciamento de Nucleotídeos em Larga Escala
Mutação
Fenilalanina Amônia-Liase/genética
Pigmentação/genética
Reguladores de Crescimento de Planta/genética
Proteínas de Plantas/genética
Tubérculos/genética
Tubérculos/metabolismo
RNA de Plantas/genética
Fatores de Transcrição/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anthocyanins); 0 (Glucosides); 0 (Plant Growth Regulators); 0 (Plant Proteins); 0 (RNA, Plant); 0 (Transcription Factors); 6988-81-4 (petunidin-3-glucoside); 8H1WZY9R6P (pelargonidin-3-glucoside); 9035-51-2 (Cytochrome P-450 Enzyme System); EC 1.14.- (flavonoid 3',5'-hydroxylase); EC 4.3.1.24 (Phenylalanine Ammonia-Lyase); EC 6.2.1.- (Coenzyme A Ligases); EC 6.2.1.12 (4-coumarate-CoA ligase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191406


  7 / 10839 MEDLINE  
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[PMID]:29037704
[Au] Autor:Mazewski C; Liang K; Gonzalez de Mejia E
[Ad] Endereço:Department of Food Science and Human Nutrition, University of Illinois at Urbana-Champaign, USA. Electronic address: cmazews2@illlinois.edu.
[Ti] Título:Comparison of the effect of chemical composition of anthocyanin-rich plant extracts on colon cancer cell proliferation and their potential mechanism of action using in vitro, in silico, and biochemical assays.
[So] Source:Food Chem;242:378-388, 2018 Mar 01.
[Is] ISSN:0308-8146
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The objective was to compare the anti-proliferative effect of anthocyanin-rich plant extracts on human colon cancer cells and determine their mechanism of action. Eleven extracts were tested: red (RG) and purple grape, purple sweet potato, purple carrot, black and purple bean, black lentil (BL), black peanut, sorghum (SH), black rice, and blue wheat. HCT-116 and HT-29 inhibition correlated with total phenolics (r=0.87 and 0.77, respectively), delphinidin-3-O-glucoside concentration with HT-29 inhibition (r=0.69). The concentration inhibition fifty (IC ) for BL, SH, RG on HT-29 and HCT-116 cell proliferation ranged 0.9-2.0mg/mL. Extracts decreased expression of anti-apoptotic proteins (survivin, cIAP-2, XIAP), induced apoptosis, and arrested cells in G1. Anthocyanins exhibited tyrosine kinase inhibitory potential in silico and biochemically; cyanidin-3-O-glucoside had one of the highest binding affinities with all kinases, especially ABL1 (-8.5kcal/mol). Cyanidin-3-O-glucoside and delphinidin-3-O-glucoside inhibited EGFR (IC =0.10 and 2.37µM, respectively). Cyanidin-3-O-glucoside was the most potent anthocyanin on kinase inhibition.
[Mh] Termos MeSH primário: Antocianinas/farmacologia
Proliferação Celular/efeitos dos fármacos
Neoplasias do Colo/tratamento farmacológico
Extratos Vegetais/farmacologia
[Mh] Termos MeSH secundário: Neoplasias do Colo/fisiopatologia
Glucosídeos/farmacologia
Células HCT116
Células HT29
Seres Humanos
Fenóis/farmacologia
Extratos Vegetais/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthocyanins); 0 (Glucosides); 0 (Phenols); 0 (Plant Extracts); 0 (delphinidin 3-O-glucopyranoside); 7084-24-4 (cyanidin 3-O-glucoside)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE


  8 / 10839 MEDLINE  
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[PMID]:29246220
[Au] Autor:Li H; Chen C
[Ad] Endereço:Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. lihaiges@hust.edu.cn.
[Ti] Título:Inhibition of autophagy enhances synergistic effects of Salidroside and anti-tumor agents against colorectal cancer.
[So] Source:BMC Complement Altern Med;17(1):538, 2017 Dec 16.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Various plant extracts have been suggested to be used as auxiliary agents in chemotherapy considering their anti-proliferative effect on cancer cells. However, recent reports reveal that plant extracts may function as inducers of autophagy of cancer cells. In general, autophagy confers survival advantage for cells responding to stress conditions, thus representing an important mechanism for chemo-resistance. This study was aimed to investigate the effectiveness of combined use of Salidroside (Sal, a phenylpropanoid glycosides from Rhodiola rosea L) with anti-tumor agents against colorectal cancer (CRC) cells, and moreover to evaluate the potential role of autophagy in the combined therapy. METHODS: CRC cells, HCT-116, were incubated with Sal alone or in combination with conventional chemotherapy agents including oxaliplatin (OXA), 5-fluorouracil (5-FU) and Doxorubicin (ADM). Cell proliferative characteristics were evaluated by cell viability and apoptosis rate. The protein expression was assessed by Immunofluorescent and Western blot assays. RESULTS: Sal, alone or in combination with anti-tumor agents, increased expression of autophagic biomarkers, including LC3B and Becline-1, suggesting an autophagy induction. Except for the up-regulation of p-AMPK, p-mTOR, p-NF-κB (p65), TGF-ß, p-JAK2 and p-STAT3 were down-regulated by Sal. Because autophagy is positively correlated with the activation of AMPK/mTOR, NF-κB, TGFß1 and JAK2/STAT3 cascades, the autophagy induced by Sal may associate with AMPK activation. Indeed, blockage of AMPK signaling via Compound C or AMPK knockdown inhibited the autophagy. The blockage of AMPK signaling or a direct inhibition of autophagy via 3-MA increased effectiveness of combined use of Sal with anti-tumor agents against CRC. CONCLUSIONS: Inhibition of autophagy enhances synergistic effects of Sal and anti-tumor agents against colorectal cancer. This study provides experimental evidence and theoretical reference for improvement of a novel chemotherapy treatment protocol.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Autofagia/efeitos dos fármacos
Neoplasias Colorretais/metabolismo
Glucosídeos/farmacologia
Fenóis/farmacologia
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/metabolismo
Apoptose/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Sinergismo Farmacológico
Células HCT116
Seres Humanos
Rhodiola
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Glucosides); 0 (Phenols); EC 2.7.11.31 (AMP-Activated Protein Kinases); M983H6N1S9 (rhodioloside)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-2046-z


  9 / 10839 MEDLINE  
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[PMID]:28467382
[Au] Autor:Chang NF; Chen YS; Lin YJ; Tai TH; Chen AN; Huang CH; Lin CC
[Ad] Endereço:Department of Cosmetic Science, Providence University, 200, Sec. 7, Taiwan Boulevard, Shalu Dist., Taichung 43301, Taiwan. nfchang@pu.edu.tw.
[Ti] Título:Study of Hydroquinone Mediated Cytotoxicity and Hypopigmentation Effects from UVB-Irradiated Arbutin and DeoxyArbutin.
[So] Source:Int J Mol Sci;18(5), 2017 May 03.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Arbutin (Arb) and deoxyArbutin (dA) are both effective hypopigmentation agents. However, they are glucoside derivatives of hydroquinone (HQ), which may be decayed into HQ under higher energy environments. Therefore, safety and toxicity are very important issues when considering the usage of these compounds. However, no study has verified the properties of Ultra-Violet B (UVB)-irradiated Arb and dA. In this work, we investigated the cytotoxicity and hypopigmentation effects of UVB-irradiated Arb and dA in Detroit 551 human fibroblast cells and B16-F10 mouse melanoma cells. The results showed that UVB-irradiated Arb and dA have strong cytotoxicity for the fibroblast cells, especially for dA, the caspase-3 is also activated by the treatment of UVB-irradiated dA in Detroit 551 cells. The results correlated with the produced HQ. In addition, UVB-irradiated Arb and dA suppressed the production of melanin in melanoma cells; this is due to the release of HQ that compensates for the UVB triggered Arb and dA decomposition.
[Mh] Termos MeSH primário: Arbutina/análogos & derivados
Sobrevivência Celular/efeitos dos fármacos
Hidroquinonas/toxicidade
Hipopigmentação/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Arbutina/efeitos da radiação
Arbutina/toxicidade
Caspase 3/efeitos dos fármacos
Células Cultivadas
Fibroblastos/efeitos dos fármacos
Glucosídeos
Seres Humanos
Hidroquinonas/efeitos da radiação
Melaninas/antagonistas & inibidores
Melanócitos/efeitos dos fármacos
Melanoma Experimental
Camundongos
Raios Ultravioleta
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucosides); 0 (Hydroquinones); 0 (Melanins); C5INA23HXF (Arbutin); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (Caspase 3); RG969BY5EN (deoxyarbutin); XV74C1N1AE (hydroquinone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:29292089
[Au] Autor:Yu X; Fan Z; Han Y; Zhang D; Xu L; Wang M; Yang Q; Li H; Zhou M; Zhang L; Sun G; Bai X; Li J; Wang H
[Ad] Endereço:Otolaryngology-Head and Neck Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China; Shandong Provincial Key Laboratory of Otology, Jinan, China; Shandong Institute of Otolaryngology, Jinan, China.
[Ti] Título:Paeoniflorin reduces neomycin-induced ototoxicity in hair cells by suppression of reactive oxygen species generation and extracellularly regulated kinase signalization.
[So] Source:Toxicol Lett;285:9-19, 2018 Mar 15.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The present study was designed to investigate the effect of paeoniflorin (PF) on neomycin-induced ototoxicity in hair cells (HCs). Here, we took advantage of C57BL/6 mice and cochlear explants culture to determine the role of PF in vivo and in vitro. We demonstrated that neomycin exposure induced severe hearing loss and HC damage, which was mediated by activated mitochondrial apoptosis pathway, promoted extracellular signal-regulated kinase (ERK) signaling as well as enhanced reactive oxygen species (ROS) generation in HCs. Interestingly, we found that PF pretreatment significantly alleviated neomycin-induced hearing loss, attenuated HC injury and decreased HC apoptosis caused by neomycin. Mechanistic studies revealed that PF could decrease cellular ROS levels, suppress the activation of ERK signaling and, subsequently, mitigate the imbalance of mitochondrial apoptotic pathway, thus protecting HCs from neomycin-induced apoptosis. This study indicates that PF may serve as an antioxidative and anti-apoptotic agent to prevent hearing loss caused by neomycin.
[Mh] Termos MeSH primário: Antioxidantes/uso terapêutico
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Glucosídeos/uso terapêutico
Células Ciliadas Auditivas/efeitos dos fármacos
Perda Auditiva/prevenção & controle
Monoterpenos/uso terapêutico
Neomicina/toxicidade
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Antioxidantes/administração & dosagem
Apoptose/efeitos dos fármacos
Células Cultivadas
Potenciais Evocados Auditivos do Tronco Encefálico/efeitos dos fármacos
Glucosídeos/administração & dosagem
Células Ciliadas Auditivas/metabolismo
Células Ciliadas Auditivas/patologia
Perda Auditiva/induzido quimicamente
Perda Auditiva/metabolismo
Perda Auditiva/patologia
Camundongos Endogâmicos C57BL
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/patologia
Monoterpenos/administração & dosagem
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Glucosides); 0 (Monoterpenes); 0 (Reactive Oxygen Species); 1404-04-2 (Neomycin); 21AIQ4EV64 (peoniflorin); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE



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