Base de dados : MEDLINE
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  1 / 4051 MEDLINE  
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[PMID]:29370193
[Au] Autor:Kalita D; Holm DG; LaBarbera DV; Petrash JM; Jayanty SS
[Ad] Endereço:San Luis Valley Research Center, Department of Horticulture and Landscape Architecture, Colorado State University, Center, United States of America.
[Ti] Título:Inhibition of α-glucosidase, α-amylase, and aldose reductase by potato polyphenolic compounds.
[So] Source:PLoS One;13(1):e0191025, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diabetes mellitus is a chronic disease that is becoming a serious global health problem. Diabetes has been considered to be one of the major risks of cataract and retinopathy. Synthetic and natural product inhibitors of carbohydrate degrading enzymes are able to reduce type 2 diabetes and its complications. For a long time, potatoes have been portrayed as unhealthy for diabetic patients by some nutritionist due to their high starch content. However, purple and red potato cultivars have received considerable attention from consumers because they have high levels of polyphenolic compounds that have potent antioxidant activities. In this study, we screened the total phenolics (TP) and total anthocyanins (TA) and analyzed the phenolic and anthocyanin compounds in selected potato cultivars and advanced selections with distinct flesh colors (purple, red, yellow and white). Purple and red potato cultivars had higher levels of TP and TA than tubers with other flesh colors. Chlorogenic acid is the predominant phenolic acid, and major anthocyanin is composed of the derivatives of petunidin, peonidin, malvidin and pelargonidin. We tested the potential inhibitory effect of potato extracts on the activities of α-amylase and α-glucosidase, which were targeted to develop antidiabetic therapeutic agents. We also measured inhibitory effect of potato extracts on aldose reductase (AR) which is a key enzyme that has been a major drug target for the development of therapies to treat diabetic complications. Purple flesh tubers extract showed the most effective inhibition of α-amylase, α-glucosidase, and aldose reductase with IC50 values 25, 42, and 32 µg/ml, respectively. Kinetic studies showed that anthocyanins are noncompetitive inhibitors of these enzymes, whereas phenolic acids behaved as mixed inhibitors for α-amylase and α-glucosidase and noncompetitive inhibitors for AR. This study supports the development of a positive and healthful image of potatoes, which is an important issue for consumers.
[Mh] Termos MeSH primário: Aldeído Redutase/antagonistas & inibidores
Inibidores Enzimáticos/farmacologia
Polifenóis/farmacologia
Solanum tuberosum/química
alfa-Amilases/antagonistas & inibidores
alfa-Glucosidases/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antocianinas/análise
Antocianinas/farmacologia
Cromatografia Líquida
Espectrometria de Massas
Polifenóis/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anthocyanins); 0 (Enzyme Inhibitors); 0 (Polyphenols); EC 1.1.1.21 (Aldehyde Reductase); EC 3.2.1.1 (alpha-Amylases); EC 3.2.1.20 (alpha-Glucosidases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191025


  2 / 4051 MEDLINE  
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[PMID]:29374975
[Au] Autor:Wang B; Liu T; Wu Z; Zhang L; Sun J; Wang X
[Ad] Endereço:a School of Medicine and Life Sciences , University of Jinan-Shandong Academy of Medical Sciences , Jinan , China.
[Ti] Título:Synthesis and biological evaluation of stilbene derivatives coupled to NO donors as potential antidiabetic agents.
[So] Source:J Enzyme Inhib Med Chem;33(1):416-423, 2018 Dec.
[Is] ISSN:1475-6374
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The work is focused on the design of drugs that prevent and treat diabetes and its complications. A novel class of stilbene derivatives were prepared by coupling NO donors of alkyl nitrate and were fully characterised by NMR and other techniques. These compounds were tested in vitro activity, including α-glucosidase inhibitory activity, aldose reductase (AR) inhibitory activity and advanced glycation end products (AGEs) formation inhibitory activity. A class of modified compounds could play a significant effect for treatment of diabetic complications. Target compounds 3e and 7c offered a potential drug design concept for the development of therapeutic or preventive agents for diabetes and its complications.
[Mh] Termos MeSH primário: Complicações do Diabetes/tratamento farmacológico
Diabetes Mellitus Experimental/tratamento farmacológico
Inibidores Enzimáticos/farmacologia
Hipoglicemiantes/farmacologia
Nitratos/farmacologia
Estilbenos/farmacologia
[Mh] Termos MeSH secundário: Aldeído Redutase/antagonistas & inibidores
Aldeído Redutase/metabolismo
Animais
Complicações do Diabetes/metabolismo
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/metabolismo
Relação Dose-Resposta a Droga
Desenho de Drogas
Inibidores Enzimáticos/síntese química
Inibidores Enzimáticos/química
Produtos Finais de Glicação Avançada/antagonistas & inibidores
Produtos Finais de Glicação Avançada/metabolismo
Hipoglicemiantes/síntese química
Hipoglicemiantes/química
Camundongos
Camundongos Endogâmicos
Estrutura Molecular
Nitratos/química
Óxido Nítrico/metabolismo
Estilbenos/síntese química
Estilbenos/química
Estreptozocina
Relação Estrutura-Atividade
alfa-Glucosidases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Glycation End Products, Advanced); 0 (Hypoglycemic Agents); 0 (Nitrates); 0 (Stilbenes); 31C4KY9ESH (Nitric Oxide); 5W494URQ81 (Streptozocin); EC 1.1.1.21 (Aldehyde Reductase); EC 3.2.1.20 (alpha-Glucosidases)
[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:180130
[St] Status:MEDLINE
[do] DOI:10.1080/14756366.2018.1425686


  3 / 4051 MEDLINE  
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[PMID]:29190815
[Au] Autor:Thiagarajan D; O' Shea K; Sreejit G; Ananthakrishnan R; Quadri N; Li Q; Schmidt AM; Gabbay K; Ramasamy R
[Ad] Endereço:Diabetes Research Program, Department of Medicine, New York University Langone Medical Center, New York, New York, United States of America.
[Ti] Título:Aldose reductase modulates acute activation of mesenchymal markers via the ß-catenin pathway during cardiac ischemia-reperfusion.
[So] Source:PLoS One;12(11):e0188981, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aldose reductase (AR: human, AKR1B1; mouse, AKR1B3), the first enzyme in the polyol pathway, plays a key role in mediating myocardial ischemia/reperfusion (I/R) injury. In earlier studies, using transgenic mice broadly expressing human AKR1B1 to human-relevant levels, mice devoid of Akr1b3, and pharmacological inhibitors of AR, we demonstrated that AR is an important component of myocardial I/R injury and that inhibition of this enzyme protects the heart from I/R injury. In this study, our objective was to investigate if AR modulates the ß-catenin pathway and consequent activation of mesenchymal markers during I/R in the heart. To test this premise, we used two different experimental models: in vivo, Akr1b3 null mice and wild type C57BL/6 mice (WT) were exposed to acute occlusion of the left anterior descending coronary artery (LAD) followed by recovery for 48 hours or 28 days, and ex-vivo, WT and Akr1b3 null murine hearts were perfused using the Langendorff technique (LT) and subjected to 30 min of global (zero-flow) ischemia followed by 60 min of reperfusion. Our in vivo results reveal reduced infarct size and improved functional recovery at 48 hours in mice devoid of Akr1b3 compared to WT mice. We demonstrate that the cardioprotection observed in Akr1b3 null mice was linked to acute activation of the ß-catenin pathway and consequent activation of mesenchymal markers and genes linked to fibrotic remodeling. The increased activity of the ß-catenin pathway at 48 hours of recovery post-LAD was not observed at 28 days post-infarction, thus indicating that the observed increase in ß-catenin activity was transient in the mice hearts devoid of Akr1b3. In ex vivo studies, inhibition of ß-catenin blocked the cardioprotection observed in Akr1b3 null mice hearts. Taken together, these data indicate that AR suppresses acute activation of ß-catenin and, thereby, blocks consequent induction of mesenchymal markers during early reperfusion after myocardial ischemia. Inhibition of AR might provide a therapeutic opportunity to optimize cardiac remodeling after I/R injury.
[Mh] Termos MeSH primário: Aldeído Redutase/metabolismo
Biomarcadores/metabolismo
Mesoderma/metabolismo
Traumatismo por Reperfusão Miocárdica/metabolismo
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Aldeído Redutase/genética
Animais
Regulação da Expressão Gênica
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fator de Crescimento Transformador beta2/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Tgfb2 protein, mouse); 0 (Transforming Growth Factor beta2); 0 (beta Catenin); EC 1.1.1.21 (Aldehyde Reductase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188981


  4 / 4051 MEDLINE  
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[PMID]:29049180
[Au] Autor:Jiang X; Fan X; Wu R; Geng F; Hu C
[Ad] Endereço:aNursing Department, Cangzhou Central Hospital, Cangzhou bDepartment of Emergency Medicine, Xianxian County people's Hospital, Xianxian cDepartment of Third Pediatrics dSecond Department of Internal Medicine eResearch Department, Cangzhou Central Hospital, Cangzhou, Hebei, China.
[Ti] Título:The effect of care intervention for obese patients with type II diabetes.
[So] Source:Medicine (Baltimore);96(42):e7524, 2017 Oct.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The incidence of type II diabetes mellitus (T2DM) is increasing worldwide and affecting the quality of people's life. This study was designed to evaluate the effect of care intervention on body weight and glycemic parameters in obese T2DM patients.One hundred twenty-six obese T2DM cases were randomly divided into 2 groups. Patients in control group received conventional care, while patients in the intervention group received dietary, exercise, and psychology interventions on the basis of conventional care. Twelve months follow-up was performed to compare the changes of body weight and glycemic parameters in the 2 groups.There were 119 patients completing the research, 60 in the intervention group and 59 in control group. The levels of fasting plasma glucose (FPG), 2 hours postprandial blood glucose (PBG2 h), hemoglobin A1c (HbA1c), and aldose reductase (AR) were all significantly decreased (all, P < .05) in intervention group compared with the control group after 12 months follow-up. Moreover, the body weight and BMI (body mass index) were also significantly reduced in intervention group, and the weight loss was significantly higher in intervention group than that in control group during the follow-up.To implement care intervention for obese T2DM patients could strengthen the management of blood glucose, reduce body weight and complications.
[Mh] Termos MeSH primário: Terapia Comportamental/métodos
Diabetes Mellitus Tipo 2/terapia
Dieta para Diabéticos/métodos
Terapia por Exercício/métodos
Obesidade/terapia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Aldeído Redutase/sangue
Glicemia/análise
Índice de Massa Corporal
Peso Corporal
Terapia Combinada
Diabetes Mellitus Tipo 2/complicações
Diabetes Mellitus Tipo 2/psicologia
Jejum/sangue
Feminino
Seguimentos
Hemoglobina A Glicada/análise
Seres Humanos
Masculino
Meia-Idade
Obesidade/complicações
Obesidade/psicologia
Período Pós-Prandial
Resultado do Tratamento
Perda de Peso
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Glycated Hemoglobin A); 0 (hemoglobin A1c protein, human); EC 1.1.1.21 (Aldehyde Reductase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171020
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007524


  5 / 4051 MEDLINE  
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[PMID]:28938395
[Au] Autor:Pal PB; Sonowal H; Shukla K; Srivastava SK; Ramana KV
[Ad] Endereço:Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas 77555.
[Ti] Título:Aldose Reductase Mediates NLRP3 Inflammasome-Initiated Innate Immune Response in Hyperglycemia-Induced Thp1 Monocytes and Male Mice.
[So] Source:Endocrinology;158(10):3661-3675, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Despite recent studies that show oxidative stress-generated reactive oxygen species (ROS) regulate NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-mediated innate immune response in various diabetic complications, the mechanism by which ROS activate innate immune response is not well understood. We have shown previously that aldose reductase (AR), besides reducing glucose, reduces lipid aldehydes and their glutathione conjugates and participates in various oxidative stress-induced inflammatory pathways. To understand the role of AR in ROS-induced innate immune response, we have investigated the mechanism(s) by which AR activates hyperglycemia-induced NLRP3 inflammsome-initiated innate immune response in Thp1 monocytes and in streptozotocin (STZ)-induced diabetic mice. In Thp1 monocytes, inhibition or ablation of AR prevented high-glucose-induced activation of NLRP3 inflammasome and caspase-1 and release of the innate immune cytokines interleukin (IL)-1ß and IL-18. AR inhibition in Thp1 cells also prevented the high-glucose-induced generation of ROS, influx of Ca2+, efflux of K+, and activation of Lyn, Syk, and PI3K. Furthermore, the AR inhibitor fidarestat prevented the expression of NLRP inflammasome components in STZ-induced diabetic mouse heart and aorta, and also prevented the release of various cytokines in the serum. Collectively, our data suggest that AR regulates hyperglycemia-induced NLRP3 inflammasome-mediated innate immune response by altering the ROS/Lyn/Syk/PI3K/Ca2+/K+ signals.
[Mh] Termos MeSH primário: Aldeído Redutase/genética
Diabetes Mellitus Experimental/imunologia
Hiperglicemia/imunologia
Imunidade Inata/imunologia
Inflamassomos/imunologia
Monócitos/imunologia
Proteína 3 que Contém Domínio de Pirina da Família NLR/imunologia
Estresse Oxidativo/imunologia
[Mh] Termos MeSH secundário: Aldeído Redutase/metabolismo
Animais
Cálcio/metabolismo
Linhagem Celular
Sobrevivência Celular
Citocinas/imunologia
Diabetes Mellitus Experimental/metabolismo
Ensaio de Imunoadsorção Enzimática
Técnicas de Silenciamento de Genes
Seres Humanos
Hiperglicemia/metabolismo
Immunoblotting
Interleucina-1beta/imunologia
Masculino
Camundongos
Monócitos/metabolismo
RNA Interferente Pequeno
Espécies Reativas de Oxigênio/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (IL1B protein, human); 0 (Inflammasomes); 0 (Interleukin-1beta); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (Nlrp3 protein, mouse); 0 (RNA, Small Interfering); 0 (Reactive Oxygen Species); EC 1.1.1.21 (Aldehyde Reductase); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00294


  6 / 4051 MEDLINE  
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[PMID]:28935265
[Au] Autor:El-Sayed S; Metwally K; El-Shanawani AA; Abdel-Aziz LM; El-Rashedy AA; Soliman MES; Quattrini L; Coviello V; la Motta C
[Ad] Endereço:Department of Medicinal Chemistry, Faculty of Pharmacy, Zagazig University, Zagazig, Egypt.
[Ti] Título:Quinazolinone-based rhodanine-3-acetic acids as potent aldose reductase inhibitors: Synthesis, functional evaluation and molecular modeling study.
[So] Source:Bioorg Med Chem Lett;27(20):4760-4764, 2017 10 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A series of quinazolinone-based rhodanine-3-acetic acids was synthesized and tested for in vitro aldose reductase inhibitory activity. All the target compounds displayed nanomolar activity against the target enzyme. Compounds 3a, 3b, and 3e exhibited almost 3-fold higher activity as compared to the only marketed reference drug epalrestat. Structure-activity relationship studies indicated that bulky substituents at the 3-phenyl ring of the quinazolinone moiety are generally not tolerated in the active site of the enzyme. Insertion of a methoxy group on the central benzylidene ring was found to have a variable effect on ALR-2 activity depending on the nature of peripheral quinazolinone ring substituents. Removal of the acetic acid moiety led to inactive or weakly active target compounds. Docking and molecular dynamic simulations of the most active rhodanine-3-acetic acid derivatives were also carried out, to provide the basis for further structure-guided design of novel inhibitors.
[Mh] Termos MeSH primário: Aldeído Redutase/antagonistas & inibidores
Inibidores Enzimáticos/síntese química
Quinazolinonas/química
Rodanina/química
[Mh] Termos MeSH secundário: Ácido Acético/química
Aldeído Redutase/metabolismo
Sítios de Ligação
Inibidores Enzimáticos/metabolismo
Concentração Inibidora 50
Simulação de Acoplamento Molecular
Rodanina/análogos & derivados
Rodanina/síntese química
Rodanina/metabolismo
Relação Estrutura-Atividade
Termodinâmica
Tiazolidinas/química
Tiazolidinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Quinazolinones); 0 (Thiazolidines); 424DV0807X (epalrestat); 7O50LKL2G8 (Rhodanine); EC 1.1.1.21 (Aldehyde Reductase); Q40Q9N063P (Acetic Acid)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE


  7 / 4051 MEDLINE  
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[PMID]:28922901
[Au] Autor:Yamamoto K; Ozakiya Y; Uno T
[Ad] Endereço:Department of Bioscience and Biotechnology, Kyushu University Graduate School, 6-10-1 Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan.
[Ti] Título:Localization of an Aldo-Keto Reductase (AKR2E4) in the Silkworm Bombyx mori (Lepidoptera: Bombycidae).
[So] Source:J Insect Sci;17(5), 2017 Sep 01.
[Is] ISSN:1536-2442
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aldo-keto reductase AKR2E4 reduces 3-dehydroecdysone to ecdysone in the silkworm Bombyx mori L. In this study, a quantitative polymerase chain reaction analysis revealed that the level of AKR2E4 mRNA was higher in the testes than in other tissues, and a western immunoblot analysis revealed that the AKR2E4 content in the testes was stage-specific from the fifth larval instar to the pupal stage. Immunohistochemical analysis showed that the AKR2E4 protein was present in cyst cells associated with sperm cells and spermatocytes. These results indicate that AKR2E4 plays an important role in 3-dehydroecdysone conversion to ecdysone and spermatogenesis in silkworm testes.
[Mh] Termos MeSH primário: Aldeído Redutase/genética
Bombyx/enzimologia
Bombyx/genética
Proteínas de Insetos/genética
[Mh] Termos MeSH secundário: Aldeído Redutase/metabolismo
Aldo-Ceto Redutases
Animais
Bombyx/crescimento & desenvolvimento
Proteínas de Insetos/metabolismo
Larva/enzimologia
Larva/crescimento & desenvolvimento
Masculino
Especificidade de Órgãos
Pupa/enzimologia
Pupa/crescimento & desenvolvimento
Reação em Cadeia da Polimerase em Tempo Real
Testículo/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insect Proteins); EC 1.1.1.- (Aldo-Keto Reductases); EC 1.1.1.21 (Aldehyde Reductase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1093/jisesa/iex071


  8 / 4051 MEDLINE  
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[PMID]:28856935
[Au] Autor:Misuri L; Cappiello M; Balestri F; Moschini R; Barracco V; Mura U; Del-Corso A
[Ad] Endereço:a Department of Biology, Biochemistry Unit , University of Pisa , Pisa , Italy.
[Ti] Título:The use of dimethylsulfoxide as a solvent in enzyme inhibition studies: the case of aldose reductase.
[So] Source:J Enzyme Inhib Med Chem;32(1):1152-1158, 2017 Dec.
[Is] ISSN:1475-6374
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aldose reductase (AR) is an enzyme devoted to cell detoxification and at the same time is strongly involved in the aetiology of secondary diabetic complications and the amplification of inflammatory phenomena. AR is subjected to intense inhibition studies and dimethyl sulfoxide (DMSO) is often present in the assay mixture to keep the inhibitors in solution. DMSO was revealed to act as a weak but well detectable AR differential inhibitor, acting as a competitive inhibitor of the L-idose reduction, as a mixed type of non-competitive inhibitor of HNE reduction and being inactive towards 3-glutathionyl-4-hydroxynonanal transformation. A kinetic model of DMSO action with respect to differently acting inhibitors was analysed. Three AR inhibitors, namely the flavonoids neohesperidin dihydrochalcone, rutin and phloretin, were used to evaluate the effects of DMSO on the inhibition studies on the reduction of L-idose and HNE.
[Mh] Termos MeSH primário: Aldeído Redutase/antagonistas & inibidores
Dimetil Sulfóxido/farmacologia
Inibidores Enzimáticos/farmacologia
[Mh] Termos MeSH secundário: Aldeído Redutase/isolamento & purificação
Aldeído Redutase/metabolismo
Dimetil Sulfóxido/síntese química
Dimetil Sulfóxido/química
Relação Dose-Resposta a Droga
Inibidores Enzimáticos/síntese química
Inibidores Enzimáticos/química
Seres Humanos
Proteínas Recombinantes/isolamento & purificação
Proteínas Recombinantes/metabolismo
Solventes/síntese química
Solventes/química
Solventes/farmacologia
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Recombinant Proteins); 0 (Solvents); EC 1.1.1.21 (Aldehyde Reductase); YOW8V9698H (Dimethyl Sulfoxide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1080/14756366.2017.1363744


  9 / 4051 MEDLINE  
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[PMID]:28842479
[Au] Autor:Johnson ZI; Doolittle AC; Snuggs JW; Shapiro IM; Le Maitre CL; Risbud MV
[Ad] Endereço:From the Department of Orthopaedic Surgery, Thomas Jefferson University, Philadelphia, Pennsylvania 19107 and.
[Ti] Título:TNF-α promotes nuclear enrichment of the transcription factor TonEBP/NFAT5 to selectively control inflammatory but not osmoregulatory responses in nucleus pulposus cells.
[So] Source:J Biol Chem;292(42):17561-17575, 2017 Oct 20.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intervertebral disc degeneration (IDD) causes chronic back pain and is linked to production of proinflammatory molecules by nucleus pulposus (NP) and other disc cells. Activation of tonicity-responsive enhancer-binding protein (TonEBP)/NFAT5 by non-osmotic stimuli, including proinflammatory molecules, occurs in cells involved in immune response. However, whether inflammatory stimuli activate TonEBP in NP cells and whether TonEBP controls inflammation during IDD is unknown. We show that TNF-α, but not IL-1ß or LPS, promoted nuclear enrichment of TonEBP protein. However, TNF-α-mediated activation of TonEBP did not cause induction of osmoregulatory genes. RNA sequencing showed that 8.5% of TNF-α transcriptional responses were TonEBP-dependent and identified genes regulated by both TNF-α and TonEBP. These genes were over-enriched in pathways and diseases related to inflammatory response and inhibition of matrix metalloproteases. Based on RNA-sequencing results, we further investigated regulation of novel TonEBP targets , , and TonEBP acted synergistically with TNF-α and LPS to induce -proximal promoter activity. Interestingly, this regulation required a highly conserved NF-κB-binding site but not a predicted TonE, suggesting cross-talk between these two members of the Rel family. Finally, analysis of human NP tissue showed that expression correlated with canonical osmoregulatory targets , , and , supporting findings that the inflammatory milieu during IDD does not interfere with TonEBP osmoregulation. In summary, whereas TonEBP participates in the proinflammatory response to TNF-α, therapeutic strategies targeting this transcription factor for treatment of disc disease must spare osmoprotective, prosurvival, and matrix homeostatic activities.
[Mh] Termos MeSH primário: Disco Intervertebral/metabolismo
Osmorregulação
Fatores de Transcrição/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Aldeído Redutase/biossíntese
Aldeído Redutase/genética
Animais
Linhagem Celular
Quimiocinas CXC/biossíntese
Quimiocinas CXC/genética
Criança
Pré-Escolar
Regulação da Expressão Gênica/efeitos dos fármacos
Proteínas de Choque Térmico/biossíntese
Proteínas de Choque Térmico/genética
Seres Humanos
Lactente
Inflamação/genética
Inflamação/metabolismo
Inflamação/patologia
Disco Intervertebral/patologia
Degeneração do Disco Intervertebral/genética
Degeneração do Disco Intervertebral/metabolismo
Degeneração do Disco Intervertebral/patologia
Lipopolissacarídeos/toxicidade
Masculino
Glicoproteínas de Membrana/biossíntese
Glicoproteínas de Membrana/genética
Proteínas de Membrana Transportadoras/biossíntese
Proteínas de Membrana Transportadoras/genética
Meia-Idade
Ratos
Simportadores/biossíntese
Simportadores/genética
Fatores de Transcrição/genética
Fator de Necrose Tumoral alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokines, CXC); 0 (Heat-Shock Proteins); 0 (Lipopolysaccharides); 0 (Membrane Glycoproteins); 0 (Membrane Transport Proteins); 0 (NFAT5 protein, human); 0 (Nfat5 protein, rat); 0 (Symporters); 0 (Transcription Factors); 0 (Tumor Necrosis Factor-alpha); 146890-04-2 (SLC5A3 protein, human); 148686-53-7 (taurine transporter); EC 1.1.1.21 (AKR1B1 protein, human); EC 1.1.1.21 (Akr1b1 protein, rat); EC 1.1.1.21 (Aldehyde Reductase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171028
[Lr] Data última revisão:
171028
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170827
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.790378


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[PMID]:28802633
[Au] Autor:Xiu ZM; Wang LP; Fu J; Xu J; Liu L
[Ad] Endereço:Center for Pharmacological Evaluation and Research, Shanghai Institute of Pharmaceutical Industry, 1111 Zhongshan North Road, Shanghai 200437, PR China; Changchun BC&HC Pharmaceutical Technology CO., Ltd, 668 Chuangxin road, Changchun 130012, PR China.
[Ti] Título:1-Acetyl-5-phenyl-1H-pyrrol-3-ylacetate: An aldose reductase inhibitor for the treatment of diabetic nephropathy.
[So] Source:Bioorg Med Chem Lett;27(18):4482-4487, 2017 09 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Diabetic nephropathy (DN) is the most common and serious complication in diabetes mellitus, but the efficacy of available strategies for preventing this disorder remains poor. The aim of this study was to investigate the possible beneficial effects of 1-acetyl-5-phenyl-1H-pyrrol-3-ylacetate (APPA), an aldose reductase inhibitor, on DN. In the present study, a model of rat glomerular mesangial cells (HBZY-1) damaged by high glucose was used to confirm the protective effects of APPA in vitro. Then, a rat model of streptozotocin-induced diabetes was used to assess the effects of APPA in vivo. APPA increased viability and reduced apoptosis in HBZY-1 cells. In vivo, APPA improved the signs of DN as determined by measurements of blood glucose, urinary microalbumin, serum total antioxidant capacity, serum catalase activity, serum glutathione levels, and serum total superoxide dismutase activity. Hematoxylin and eosin staining of kidney tissue confirmed the protective effect. Moreover, APPA reduced the levels of transforming growth factor-ß1, collagen IV, and laminin in HBZY-1cells incubated in high glucose, and in serum in DN rats. In summary, APPA can effectively prevent apoptosis and the symptoms of streptozotocin-induced diabetes by inhibiting the polyol pathway in rats. This suggests that APPA could be a potential drug in treating DN.
[Mh] Termos MeSH primário: Acetatos/farmacologia
Aldeído Redutase/antagonistas & inibidores
Nefropatias Diabéticas/tratamento farmacológico
Inibidores Enzimáticos/farmacologia
Pirróis/farmacologia
[Mh] Termos MeSH secundário: Acetatos/síntese química
Acetatos/química
Aldeído Redutase/metabolismo
Animais
Apoptose/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Nefropatias Diabéticas/induzido quimicamente
Nefropatias Diabéticas/metabolismo
Relação Dose-Resposta a Droga
Inibidores Enzimáticos/síntese química
Inibidores Enzimáticos/química
Estrutura Molecular
Pirróis/síntese química
Pirróis/química
Ratos
Estreptozocina
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1-acetyl-5-phenyl-1H-pyrrol-3-ylacetate); 0 (Acetates); 0 (Enzyme Inhibitors); 0 (Pyrroles); 5W494URQ81 (Streptozocin); EC 1.1.1.21 (Aldehyde Reductase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170814
[St] Status:MEDLINE



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