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[PMID]:29318368
[Au] Autor:Mirlohi MS; Yaghooti H; Shirali S; Aminasnafi A; Olapour S
[Ad] Endereço:Hyperlipidemia Research Center, School of Allied Medical Sciences, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
[Ti] Título:Increased levels of advanced glycation end products positively correlate with iron overload and oxidative stress markers in patients with ß-thalassemia major.
[So] Source:Ann Hematol;97(4):679-684, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The impaired biosynthesis of the ß-globin chain in ß-thalassemia leads to the accumulation of unpaired alpha globin chains, failure in hemoglobin formation, and iron overload due to frequent blood transfusion. Iron excess causes oxidative stress and massive tissue injuries. Advanced glycation end products (AGEs) are harmful agents, and their production accelerates in oxidative conditions. This study was conducted on 45 patients with major ß-thalassemia who received frequent blood transfusions and chelation therapy and were compared to 40 healthy subjects. Metabolic parameters including glycemic and iron indices, hepatic and renal functions tests, oxidative stress markers, and AGEs (carboxymethyl-lysine and pentosidine) levels were measured. All parameters were significantly increased in ß-thalassemia compared to the control except for glutathione levels. Blood glucose, iron, serum ferritin, non-transferrin-bound iron (NTBI), MDA, soluble form of low-density lipoprotein receptor, glutathione peroxidase, total reactive oxygen species (ROS), and AGE levels were significantly higher in the ß-thalassemia patients. Iron and ferritin showed a significant positive correlation with pentosidine (P < 0.01) but not with carboxymethyl-lysine. The NTBI was markedly increased in the ß-thalassemia patients, and its levels correlated significantly with both carboxymethyl-lysine and pentosidine (P < 0.05). Our findings confirm the oxidative status generated by the iron overload in ß-thalassemia major patients and highlight the enhanced formation of AGEs, which may play an important role in the pathogenesis of ß-thalassemia major.
[Mh] Termos MeSH primário: Transfusão de Sangue
Produtos Finais de Glicação Avançada/sangue
Sobrecarga de Ferro/etiologia
Estresse Oxidativo
Reação Transfusional/fisiopatologia
Talassemia beta/sangue
[Mh] Termos MeSH secundário: Adolescente
Adulto
Biomarcadores/sangue
Terapia por Quelação/efeitos adversos
Terapia Combinada/efeitos adversos
Estudos Transversais
Desferroxamina/uso terapêutico
Feminino
Seres Humanos
Irã (Geográfico)
Sobrecarga de Ferro/prevenção & controle
Masculino
Piridonas/uso terapêutico
Receptores Depuradores Classe E/sangue
Adulto Jovem
Talassemia beta/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Glycation End Products, Advanced); 0 (OLR1 protein, human); 0 (Pyridones); 0 (Scavenger Receptors, Class E); 2BTY8KH53L (deferiprone); J06Y7MXW4D (Deferoxamine)
[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:180111
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3223-3


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[PMID]:29265388
[Au] Autor:Dybkowska E; Sadowska A; Rakowska R; Debowska M; Swiderski F; Swiader K
[Ad] Endereço:Warsaw University of Life Sciences - SGGW, Faculty of Human Nutrition and Consumer Sciences, Department of Functional Food, Ecological Food and Commodities, Warsaw, Poland
[Ti] Título:Assessing polyphenols content and antioxidant activity in coffee beans according to origin and the degree of roasting
[So] Source:Rocz Panstw Zakl Hig;68(4):347-353, 2017.
[Is] ISSN:0035-7715
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Background: The roasting stage constitutes a key component in the manufacturing process of natural coffee because temperature elicits changes in bioactive compounds such as polyphenols and that Maillard-reaction compounds appear, thus affecting the product's sensory and antioxidant properties. Actual contents of these compounds may depend on which region the coffee is cultivated as well as the extent to which the beans are roasted Objectives: To determine polyphenols content and antioxidant activity in the 'Arabica' coffee type coming from various world regions of its cultivation and which have undergone industrial roasting. Also to establish which coffee, taking into account the degree of roasting (ie. light, medium and strong), is nutritionally the most beneficial Materials and Methods: The study material was natural coffee beans (100% Arabica) roasted to various degrees, as aforementioned, that had been cultivated in Brazil, Ethiopia, Columbia and India. Polyphenols were measured in the coffee beans by spectrophotometric means based on the Folin-Ciocalteu reaction, whereas antioxidant activity was measured colourimetrically using ABTS+ cat-ionic radicals Results: Polyphenol content and antioxidant activity were found to depend both on the coffee's origin and degree of roasting. Longer roasting times resulted in greater polyphenol degradation. The highest polyphenol concentrations were found in lightly roasted coffee, ranging 39.27 to 43.0 mg/g, whereas levels in medium and strongly roasted coffee respectively ranged 34.06 to 38.43 mg/g and 29.21 to 36.89 mg/g. Antioxidant activity however significantly rose with the degree of roasting, where strongly roasted coffee had higher such activity than lightly roasted coffee. This can be explained by the formation of Maillard-reaction compounds during roasting, leading then to the formation of antioxidant melanoidin compounds which, to a large extent, compensate for the decrease in polyphenols during roasting Conclusions: Polyphenols levels and antioxidant activities in the studied Arabica coffee beans that had undergone roasting depended on the cultivation region of the world. Longer roasting caused a significant decline in polyphenols compound levels (from 7.3% to 32.1%) in the coffee beans. Antioxidant activities of coffee increased with roasting, despite reduced levels of natural antioxidants. From a nutritional standpoint, the most favoured coffees are those lightly or medium roasted
[Mh] Termos MeSH primário: Antioxidantes/análise
Coffea/química
Café/química
Manipulação de Alimentos/métodos
Polifenóis/análise
[Mh] Termos MeSH secundário: Coffea/classificação
Produtos Finais de Glicação Avançada
Temperatura Alta
Seres Humanos
Sementes/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Coffee); 0 (Glycation End Products, Advanced); 0 (Polyphenols)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:29386427
[Au] Autor:Tachibana M
[Ad] Endereço:Laboratory of Biotechnology and Therapeutics, Graduate School of Pharmaceutical Sciences, Osaka University.
[Ti] Título:[The Immunosuppressive Function of Myeloid-derived Suppressor Cells Is Regulated by the HMGB1-TLR4 Axis].
[So] Source:Yakugaku Zasshi;138(2):143-148, 2018.
[Is] ISSN:1347-5231
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo: Myeloid-derived suppressor cells (MDSCs) accumulate under pathological conditions, including cancer and chronic inflammation, and they suppress various immune responses such as T cell proliferation. Although several inflammatory signals enhance the differentiation and/or function of MDSCs, it is not clear which factors regulate their differentiation and immunosuppressive function. It has been highlighted that damage-associated molecular patterns (DAMPs) play important roles in the induction of inflammation. One of the DAMPs, the high mobility group box 1 (HMGB1), is released from necrotic cells and secreted by macrophages. It has been shown that HMGB1 level is elevated in tumors and tumor-bearing hosts. It has also been reported that HMGB1 transduces intracellular signaling via several receptors, including the receptor for advanced glycation end-products (RAGE) and the toll-like receptor (TLR)4, both of which enhance the differentiation and/or function of MDSCs. However, the effects of HMGB1 on MDSCs remain unclear. In the present study, we examined the effect of HMGB1 on in vitro MDSC differentiation and immunosuppressive functions. Since murine bone marrow (BM) cells can differentiate into MDSCs upon granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulation for 4 d in vitro, we cultured murine BM cells in the presence of HMGB1 and GM-CSF. The results demonstrated that HMGB1 enhanced the suppressive activity of in vitro MDSCs, depending on TLR4, whereas lipopolysaccharide (LPS), one of the TLR4 ligands, interfered with this differentiation and immunosuppressive activity of in vitro MDSCs, depending on TLR4. Our findings thus suggest that the HMGB1-TLR4 axis enhances the immunosuppressive function of MDSCs.
[Mh] Termos MeSH primário: Células da Medula Óssea/imunologia
Proteína HMGB1/fisiologia
Imunossupressão
Transdução de Sinais/fisiologia
Receptor 4 Toll-Like/fisiologia
[Mh] Termos MeSH secundário: Alarminas
Animais
Células da Medula Óssea/citologia
Diferenciação Celular
Produtos Finais de Glicação Avançada
Seres Humanos
Inflamação/imunologia
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Alarmins); 0 (Glycation End Products, Advanced); 0 (HMGB1 Protein); 0 (Toll-Like Receptor 4)
[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.17-00158


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[PMID]:27776915
[Au] Autor:Mendler M; Riedinger C; Schlotterer A; Volk N; Fleming T; Herzig S; Nawroth PP; Morcos M
[Ad] Endereço:Department of Medicine 1 and Clinical Chemistry, University of Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany. Electronic address: michael.mendler@med.uni-heidelberg.de.
[Ti] Título:Reduction in ins-7 gene expression in non-neuronal cells of high glucose exposed Caenorhabditis elegans protects from reactive metabolites, preserves neuronal structure and head motility, and prolongs lifespan.
[So] Source:J Diabetes Complications;31(2):304-310, 2017 Feb.
[Is] ISSN:1873-460X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Glucose derived metabolism generates reactive metabolites affecting the neuronal system and lifespan in C. elegans. Here, the role of the insulin homologue ins-7 and its downstream effectors in the generation of high glucose induced neuronal damage and shortening of lifespan was studied. RESULTS: In C. elegans high glucose conditions induced the expression of the insulin homologue ins-7. Abrogating ins-7 under high glucose conditions in non-neuronal cells decreased reactive oxygen species (ROS)-formation and accumulation of methylglyoxal derived advanced glycation endproducts (AGEs), prevented structural neuronal damage and normalised head motility and lifespan. The restoration of lifespan by decreased ins-7 expression was dependent on the concerted action of sod-3 and glod-4 coding for the homologues of iron-manganese superoxide dismutase and glyoxalase 1, respectively. CONCLUSIONS: Under high glucose conditions mitochondria-mediated oxidative stress and glycation are downstream targets of ins-7. This impairs the neuronal system and longevity via a non-neuronal/neuronal crosstalk by affecting sod-3 and glod-4, thus giving further insight into the pathophysiology of diabetic complications.
[Mh] Termos MeSH primário: Proteínas de Caenorhabditis elegans/antagonistas & inibidores
Proteínas de Caenorhabditis elegans/metabolismo
Caenorhabditis elegans/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Glucose/envenenamento
Lactoilglutationa Liase/metabolismo
Estresse Oxidativo
Hormônios Peptídicos/antagonistas & inibidores
Superóxido Dismutase/metabolismo
[Mh] Termos MeSH secundário: Animais
Comportamento Animal
Caenorhabditis elegans/enzimologia
Caenorhabditis elegans/crescimento & desenvolvimento
Proteínas de Caenorhabditis elegans/agonistas
Proteínas de Caenorhabditis elegans/genética
Retroalimentação Fisiológica
Técnicas de Silenciamento de Genes
Técnicas de Inativação de Genes
Produtos Finais de Glicação Avançada/metabolismo
Lactoilglutationa Liase/antagonistas & inibidores
Lactoilglutationa Liase/genética
Longevidade
Mutação
Neuroproteção
Concentração Osmolar
Hormônios Peptídicos/agonistas
Hormônios Peptídicos/genética
Hormônios Peptídicos/metabolismo
Interferência de RNA
Espécies Reativas de Oxigênio/metabolismo
Superóxido Dismutase/antagonistas & inibidores
Superóxido Dismutase/genética
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Caenorhabditis elegans Proteins); 0 (Glycation End Products, Advanced); 0 (Ins-7 protein, C elegans); 0 (Peptide Hormones); 0 (Reactive Oxygen Species); EC 1.15.1.1 (Sod-3 protein, C elegans); EC 1.15.1.1 (Superoxide Dismutase); EC 4.4.1.5 (Lactoylglutathione Lyase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:29202487
[Au] Autor:Sarabia-Sainz HM; Mata Haro V; Sarabia Sainz JA; Vázquez-Moreno L; Montfort GR
[Ad] Endereço:Laboratorio de Bioquímica de Proteínas y Glicanos Coordinación de Ciencia de los Alimentos, Centro de Investigación en Alimentación y Desarrollo A.C., Hermosillo, Sonora 83304, México.
[Ti] Título:Maillard neoglycans as inhibitors for in vitro adhesion of F4 enterotoxigenic Escherichia coli to piglet intestinal cells.
[So] Source:Acta Biochim Pol;64(4):679-686, 2017.
[Is] ISSN:1734-154X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Adhesion of enterotoxigenic (ETEC) E. coli to host intestinal cells is mediated by lectin-like fimbriae that bind to specific glycan moieties on the surfaces of enterocytes. To prevent in vitro binding of E. coli F4 fimbriae (F4 ETEC ) to piglet enterocytes, neoglycans were synthesized by the Maillard reaction conjugating lactose (Lac), galacto-oligosaccharides (GOS) or chitin oligosaccharides (Ochit) to porcine serum albumin (PSA). Neoglycans were characterized by SDS-PAGE, intrinsic tryptophan fluorescence and recognition by plant lectins, as well as by F4 ETEC variants. Electrophoretic patterns suggested the binding to PSA of 63, 13 and 2 molecules of Lac, GOS and Ochit, respectively. All neoglycans displayed quenching of tryptophan fluorescence consistent with the degree of glycation estimated by SDS-PAGE. Plant lectins recognized the neoglycans according to their specificity, whereas antigenic variants of F4 ETEC (ab, ac and ad) recognized PSA-Ochit and PSA-Lac with higher affinity than that for GOS. Neoglycans partially hindered the in vitro binding of F4 ETEC to piglet enterocytes in a dose-dependent manner. The most effective blocking was observed with PSA-Lac that partially inhibited the adhesion of bacteria to enterocytes in a dose dependent manner, as quantified by flow cytometry. Increased production of the cytokines IL-6 and TNF-α was observed in response to F4 ETEC infection of enterocytes and production was reduced in the presence of PSA-Ochit and PSA-GOS. These results suggest that neoglycans synthesized by the Maillard reaction could be useful in the prophylaxis of diarrhea in piglets.
[Mh] Termos MeSH primário: Enterócitos/efeitos dos fármacos
Enterócitos/microbiologia
Escherichia coli Enterotoxigênica/efeitos dos fármacos
Polissacarídeos/química
Polissacarídeos/farmacologia
[Mh] Termos MeSH secundário: Animais
Antibacterianos/química
Antibacterianos/farmacologia
Aderência Bacteriana/efeitos dos fármacos
Eletroforese em Gel de Poliacrilamida
Escherichia coli Enterotoxigênica/patogenicidade
Infecções por Escherichia coli/tratamento farmacológico
Infecções por Escherichia coli/microbiologia
Infecções por Escherichia coli/veterinária
Produtos Finais de Glicação Avançada/química
Intestinos/citologia
Intestinos/microbiologia
Suínos
Doenças dos Suínos/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Glycation End Products, Advanced); 0 (Polysaccharides)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.18388/abp.2017_2199


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[PMID]:28456475
[Au] Autor:Molinuevo MS; Fernández JM; Cortizo AM; McCarthy AD; Schurman L; Sedlinsky C
[Ad] Endereço:Laboratorio de Investigación en Osteopatías y Metabolismo Mineral, Facultad de Ciencias Exactas, Universidad Nacional de La Plata. 47 y 115, (1900) La Plata, Argentina.
[Ti] Título:Advanced glycation end products and strontium ranelate promote osteogenic differentiation of vascular smooth muscle cells in vitro: Preventive role of vitamin D.
[So] Source:Mol Cell Endocrinol;450:94-104, 2017 Jul 15.
[Is] ISSN:1872-8057
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Advanced glycation end products (AGE) have been demonstrated to induce the osteogenic trans-differentiation of vascular smooth muscle cells (VSMC). Strontium ranelate (SR) is an anti-osteoporotic agent that has both anti-catabolic and anabolic actions on bone tissue. However, in the last years SR has been associated with an increase of cardiovascular risk. We hypothesize that SR can increase the osteoblastic trans-differentiation of VSMC and the induction of extracellular calcifications, an effect that could be potentiated in the presence of AGE and inhibited by simultaneous administration of vitamin D. The present results of our in vitro experiments demonstrate that AGE and SR alone or in combination, stimulate L-type calcium channels, causing an increase in reactive oxygen species and activation of both ERK and NFkB, with the final effect of promoting the osteogenic shift of VSMC. Importantly, these in vitro effects of AGE and/or SR can be prevented by co-incubation with vitamin D.
[Mh] Termos MeSH primário: Diferenciação Celular/efeitos dos fármacos
Produtos Finais de Glicação Avançada/farmacologia
Músculo Liso Vascular/citologia
Miócitos de Músculo Liso/citologia
Osteogênese/efeitos dos fármacos
Tiofenos/farmacologia
Vitamina D/farmacologia
[Mh] Termos MeSH secundário: Animais
Ácido Ascórbico/farmacologia
Contagem de Células
Movimento Celular/efeitos dos fármacos
Subunidade alfa 1 de Fator de Ligação ao Core/metabolismo
Masculino
Modelos Biológicos
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
Nifedipino/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
Sulfassalazina/farmacologia
Vitamina E/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Core Binding Factor Alpha 1 Subunit); 0 (Glycation End Products, Advanced); 0 (Reactive Oxygen Species); 0 (Thiophenes); 04NQ160FRU (strontium ranelate); 1406-16-2 (Vitamin D); 1406-18-4 (Vitamin E); 3XC8GUZ6CB (Sulfasalazine); I9ZF7L6G2L (Nifedipine); PQ6CK8PD0R (Ascorbic Acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:29174818
[Au] Autor:Pei Z; Deng Q; Babcock SA; He EY; Ren J; Zhang Y
[Ad] Endereço:The Second Department of Cardiology, The Third Hospital of Nanchang, Nanchang, Jiangxi 330009, China.
[Ti] Título:Inhibition of advanced glycation endproduct (AGE) rescues against streptozotocin-induced diabetic cardiomyopathy: Role of autophagy and ER stress.
[So] Source:Toxicol Lett;284:10-20, 2018 Mar 01.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Diabetes mellitus leads to oxidative stress and contractile dysfunction in the heart. Although several rationales have been speculated, the precise mechanism behind diabetic cardiomyopathy remains elusive. This study was designed to assess the role of inhibition of advanced glycation endproducts (AGE) in streptozotocin (STZ)-induced diabetic cardiac dysfunction. Cardiac contractile function was assessed in normal C57BL/6 and STZ (200mg/kg, single injection and maintained for 2 wks)-induced diabetic mice treated with or without the AGE inhibitor aminoguanidine (50mg/kg/d in drinking water) for 2 weeks using echocardiography and IonOptix MyoCam techniques. Diabetes compromised cardiac contractile function shown as reduced fractional shortening and ejection fraction, enlarged left ventricular end systolic/diastolic diameters, decreased peak shortening, maximal velocity of shortening/relengthening, prolonged shortening and relengthening duration as well as impaired intracellular Ca homeostasis, the effects of which were alleviated or reversed by aminoguanidine treatment. Diabetes also inhibited autophagy, increased ER stress and phosphorylation of pro-hypertrophic signaling molecules Akt and mTOR, the effect of which was reversed by aminoguanidine. In vitro study revealed that methylglyoxal-derived AGE (MG-AGE) incubation in isolated cardiomyocytes promoted oxidation of sarco(endo)plasmic reticulum Ca -ATPase (SERCA2a) and production of superoxide, the effects of which were negated by the autophagy inducer rapamycin, the ER stress chaperone TUDCA or the antioxidant N-acetylcysteine. Taken together, these data revealed that inhibition of AGE formation rescues against experimental diabetes-induced cardiac remodeling and contractile dysfunction possible through regulation of autophagy and ER stress.
[Mh] Termos MeSH primário: Autofagia/efeitos dos fármacos
Diabetes Mellitus Experimental/metabolismo
Cardiomiopatias Diabéticas/prevenção & controle
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Produtos Finais de Glicação Avançada/antagonistas & inibidores
Guanidinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Diabetes Mellitus Experimental/patologia
Cardiomiopatias Diabéticas/metabolismo
Cardiomiopatias Diabéticas/patologia
Ecocardiografia
Masculino
Camundongos Endogâmicos C57BL
Contração Miocárdica/efeitos dos fármacos
Miócitos Cardíacos/efeitos dos fármacos
Estreptozocina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycation End Products, Advanced); 0 (Guanidines); 5W494URQ81 (Streptozocin); SCQ4EZQ113 (pimagedine); SY7Q814VUP (Calcium)
[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:171128
[St] Status:MEDLINE


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[PMID]:29334926
[Au] Autor:Ghelani H; Razmovski-Naumovski V; Pragada RR; Nammi S
[Ad] Endereço:School of Science and Health, Western Sydney University, Sydney, NSW, 2751, Australia.
[Ti] Título:(R)-α-Lipoic acid inhibits fructose-induced myoglobin fructation and the formation of advanced glycation end products (AGEs) in vitro.
[So] Source:BMC Complement Altern Med;18(1):13, 2018 Jan 15.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Fructose-mediated protein glycation (fructation) has been linked to an increase in diabetic and cardiovascular complications due to over consumption of high-fructose containing diets in recent times. The objective of the present study is to evaluate the protective effect of (R)-α-lipoic acid (ALA) against fructose-induced myoglobin fructation and the formation of advanced glycation end products (AGEs) in vitro. METHODS: The anti-glycation activity of ALA was determined using the formation of AGEs fluorescence intensity, iron released from the heme moiety of myoglobin and the level of fructosamine. The fructation-induced myoglobin oxidation was examined using the level of protein carbonyl content and thiol group estimation. RESULTS: The results showed that co-incubation of myoglobin (1 mg/mL), fructose (1 M) and ALA (1, 2 and 4 mM) significantly inhibited the formation of AGEs during the 30 day study period. ALA markedly decreased the levels of fructosamine, which is directly associated with the reduction of AGEs formation. Furthermore, ALA significantly reduced free iron release from myoglobin which is attributed to the protection of myoglobin from fructose-induced glycation. The results also demonstrated a significant protective effect of ALA on myoglobin oxidative damages, as seen from decreased protein carbonyl content and increased protein thiols. CONCLUSION: These findings provide new insights into the anti-glycation properties of ALA and emphasize that ALA supplementation is beneficial in the prevention of AGEs-mediated diabetic and cardiovascular complications.
[Mh] Termos MeSH primário: Frutose/metabolismo
Produtos Finais de Glicação Avançada/metabolismo
Glicosilação/efeitos dos fármacos
Mioglobina/metabolismo
Ácido Tióctico/farmacologia
[Mh] Termos MeSH secundário: Animais
Produtos Finais de Glicação Avançada/análise
Mioglobina/análise
Mioglobina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycation End Products, Advanced); 0 (Myoglobin); 30237-26-4 (Fructose); 73Y7P0K73Y (Thioctic Acid)
[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:180117
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-2076-6


  9 / 6220 MEDLINE  
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[PMID]:29244109
[Au] Autor:Zhou L; Wang W; Yang C; Zeng T; Hu M; Wang X; Li N; Sun K; Wang C; Zhou J; Ren M; Yan L
[Ad] Endereço:Department of Endocrinology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
[Ti] Título:GADD45a Promotes Active DNA Demethylation of the MMP-9 Promoter via Base Excision Repair Pathway in AGEs-Treated Keratinocytes and in Diabetic Male Rat Skin.
[So] Source:Endocrinology;159(2):1172-1186, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diabetes elevates matrix metalloproteinase (MMP)-9 levels in the skin and its keratinocytes, and activated MMP-9 impairs skin wound healing. Epigenetic regulation of the DNA methylation status within the MMP-9 promoter plays an important role in the alteration of MMP-9 expression. Our aim was to investigate the role and mechanism of growth arrest and DNA damage-inducible 45a (GADD45a), a well-known DNA demethylation regulatory protein that mediates DNA methylation, in the regulation of MMP-9 expression. In this study, we showed that GADD45a was markedly upregulated in skin tissues from patients with diabetic foot ulcers, in diabetic rats, and in human keratinocyte (HaCaT) cells exposed to advanced glycation end products. We observed a substantial positive correlation between the levels of GADD45a and MMP-9 expression. Knockdown of GADD45a ameliorated the increase in MMP-9 transcription induced by a diabetic condition by inhibiting demethylation in the MMP-9 promoter and promoted diabetic HaCaT cell migration, but GADD45a knockdown did not affect HaCaT cell proliferation or apoptosis. Additionally, we demonstrated that overexpression of GADD45a activated MMP-9 expression by inducing promoter demethylation. Moreover, we found that GADD45a binds to the promoter of MMP-9 and recruits thymine-DNA glycosylase for base excision repair-mediated demethylation in diabetic HaCaT cells and diabetic rat skin. Our results reveal a mechanism in which GADD45a is required for demethylation of the MMP-9 promoter and the induction of diabetic wound healing. The inhibition of GADD45a might be a therapeutic strategy for diabetic foot ulcers.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/fisiologia
Reparo do DNA/genética
Diabetes Mellitus Experimental/patologia
Produtos Finais de Glicação Avançada/farmacologia
Queratinócitos/patologia
Metaloproteinase 9 da Matriz/genética
Proteínas Nucleares/fisiologia
Pele/patologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Desmetilação do DNA
Diabetes Mellitus Experimental/genética
Diabetes Mellitus Experimental/metabolismo
Pé Diabético/genética
Pé Diabético/metabolismo
Pé Diabético/patologia
Epigênese Genética
Regulação Enzimológica da Expressão Gênica
Produtos Finais de Glicação Avançada/metabolismo
Seres Humanos
Queratinócitos/efeitos dos fármacos
Queratinócitos/metabolismo
Masculino
Metaloproteinase 9 da Matriz/metabolismo
Regiões Promotoras Genéticas
Ratos
Ratos Sprague-Dawley
Pele/efeitos dos fármacos
Pele/metabolismo
Cicatrização/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (GADD45A protein, human); 0 (Gadd45a protein, rat); 0 (Glycation End Products, Advanced); 0 (Nuclear Proteins); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00686


  10 / 6220 MEDLINE  
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[PMID]:29196260
[Au] Autor:Lee KJ; Yoo JW; Kim YK; Choi JH; Ha TY; Gil M
[Ad] Endereço:Department of Convergence Medicine, Asan Institute for Life Sciences, University of Ulsan College of Medicine, Asan Medical Center, Seoul 05505, Republic of Korea.
[Ti] Título:Advanced glycation end products promote triple negative breast cancer cells via ERK and NF-κB pathway.
[So] Source:Biochem Biophys Res Commun;495(3):2195-2201, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Advanced glycation end products (AGEs) are harmful compounds generated by nonspecific glycation of proteins and lipids. The accumulation of AGEs is associated with various diseases, including breast cancer. AGEs have been shown to promote a breast cancer cell line by enhancing proliferation, invasion and migration. In this study, we investigated the effect and associated mechanism of AGEs on triple negative breast cancer cells. AGEs enhanced the proliferation, tumorigenicity, invasion and migration of primary breast cancer cells. AGEs also enhanced the RNA and protein expression of matrix metalloproteinase (MMP)-9 and its gelatinase activity. Enhanced MMP-9 expression was mediated by extracellular-signal regulated kinase (ERK) and nuclear factor kappa B (NF-κB) pathways. Moreover, inhibitors of ERK and NF-κB signaling attenuated the effect of AGEs on tumorigenicity, invasion and migration of primary breast cancer cells. Taken together, we suggest that AGEs directly promote primary breast cancer cells via the ERK and NF-κB pathway, which may lead to advanced therapeutic modalities of breast cancer.
[Mh] Termos MeSH primário: Produtos Finais de Glicação Avançada/metabolismo
Sistema de Sinalização das MAP Quinases
NF-kappa B/metabolismo
Neoplasias de Mama Triplo Negativas/metabolismo
Neoplasias de Mama Triplo Negativas/patologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Seres Humanos
Invasividade Neoplásica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Glycation End Products, Advanced); 0 (NF-kappa B)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171203
[St] Status:MEDLINE



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