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[PMID]:28467723
[Au] Autor:Diaz-Morales N; Rovira-Llopis S; Bañuls C; Lopez-Domenech S; Escribano-Lopez I; Veses S; Jover A; Rocha M; Hernandez-Mijares A; Victor VM
[Ad] Endereço:1 Service of Endocrinology and Nutrition, University Hospital Doctor Peset , Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain .
[Ti] Título:Does Metformin Protect Diabetic Patients from Oxidative Stress and Leukocyte-Endothelium Interactions?
[So] Source:Antioxid Redox Signal;27(17):1439-1445, 2017 Dec 10.
[Is] ISSN:1557-7716
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Since metformin can exert beneficial vascular effects, we aimed at studying its effect on reactive oxygen species (ROS) production, antioxidant enzyme expression, levels of adhesion molecules, and leukocyte-endothelium interactions in the leukocytes from type 2 diabetic (T2D) patients. The study was carried out in 72 T2D patients (41 of whom were treated with metformin for at least 12 months at a dose of 1700 mg per day), and in 40 sex- and age-matched control subjects. Leukocytes from T2D patients exhibited enhanced levels of mitochondrial ROS and decreased mRNA levels of glutathione peroxidase 1 (gpx1) and sirtuin 3 (sirt3) with respect to controls, whereas metformin was shown to revert these effects. No changes were observed on total ROS production and the expression levels of superoxide dismutase 1 and catalase. Furthermore, increases in leukocyte-endothelial interactions and intercellular adhesion molecule-1 and P-selectin levels were found in T2D and were also restored in metformin-treated patients. Our findings raise the question of whether metformin could modulate the appearance of atherosclerosis in T2D patients and reduce vascular events by decreasing leukocyte oxidative stress through an increase in gpx1 and sirt3 expression, and undermining adhesion molecule levels and leukocyte-endothelium interactions. Antioxid. Redox Signal. 27, 1439-1445.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/tratamento farmacológico
Células Endoteliais/efeitos dos fármacos
Hipoglicemiantes/administração & dosagem
Leucócitos/efeitos dos fármacos
Metformina/administração & dosagem
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Idoso
Catalase
Adesão Celular
Diabetes Mellitus Tipo 2/genética
Diabetes Mellitus Tipo 2/metabolismo
Células Endoteliais/metabolismo
Feminino
Glutationa Peroxidase/genética
Seres Humanos
Hipoglicemiantes/farmacologia
Molécula 1 de Adesão Intercelular/metabolismo
Leucócitos/metabolismo
Masculino
Metformina/farmacologia
Meia-Idade
Selectina-P/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Sirtuína 3/genética
Superóxido Dismutase-1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypoglycemic Agents); 0 (ICAM1 protein, human); 0 (P-Selectin); 0 (Reactive Oxygen Species); 0 (SOD1 protein, human); 126547-89-5 (Intercellular Adhesion Molecule-1); 9100L32L2N (Metformin); EC 1.11.1.- (glutathione peroxidase GPX1); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase-1); EC 3.5.1.- (SIRT3 protein, human); EC 3.5.1.- (Sirtuin 3)
[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:170504
[St] Status:MEDLINE
[do] DOI:10.1089/ars.2017.7122


  2 / 16653 MEDLINE  
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[PMID]:27776018
[Au] Autor:Vartanian A; Baryshnikova M; Burova O; Afanasyeva D; Misyurin V; Belyаvsky A; Shprakh Z
[Ad] Endereço:Department of Experimental Diagnosis and Therapy of Tumors, N.N. Blokhin Russian Cancer Research Center, Moscow, Russia.
[Ti] Título:Inhibitor of vasculogenic mimicry restores sensitivity of resistant melanoma cells to DNA-damaging agents.
[So] Source:Melanoma Res;27(1):8-16, 2017 Feb.
[Is] ISSN:1473-5636
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The increasing incidence of melanoma makes this cancer an important public health problem. Therapeutic resistance is still a major obstacle to the therapy of patients with metastatic melanomas. The aim of this study was to develop the melanoma cell line resistant to DNA-alkylating agents and to elucidate the mechanisms involved in acquired drug resistance. We established a unique melanoma subline Mel MeR resistant to DNA-alkylating drug aranoza by continuous stepwise selection of the Mel Me/WT cell line with increasing concentrations of this drug. Mel MeR cells were also cross-resistant to streptozotocin or cisplatin. Here, we show that aranoza-resistant melanoma cells modulate the ABC transporter activity, upregulate the expression of PRAME, adopt a vascular-related phenotype and engage in vasculogenic mimicry. LCS1269, a vasculogenic mimicry low-molecular-weight inhibitor, reverses the sensitivity of resistant melanoma cells to DNA-damaging agents. In this study, we provide experimental evidence that LCS1269 might be considered as a new potential anticancer agent capable of overcoming multidrug resistance for DNA-damaging agents in melanoma.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/farmacologia
Carbazóis/farmacologia
Linhagem Celular Tumoral
Resistência a Medicamentos Antineoplásicos
Glicosídeos/farmacologia
Melanoma/tratamento farmacológico
Melanoma/metabolismo
Metilnitrosoureia/análogos & derivados
Neovascularização Patológica/prevenção & controle
[Mh] Termos MeSH secundário: Membro 1 da Subfamília B de Cassetes de Ligação de ATP/metabolismo
Antígenos de Neoplasias/genética
Apoptose/efeitos dos fármacos
Antígeno CD24/metabolismo
Resistência a Medicamentos Antineoplásicos/genética
Endoglina/metabolismo
Corantes Fluorescentes/metabolismo
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Receptores de Hialuronatos/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Masculino
Melanoma/irrigação sanguínea
Melanoma/genética
Metilnitrosoureia/farmacologia
Meia-Idade
Proteínas de Neoplasias/genética
Células-Tronco Neoplásicas/metabolismo
Proteínas Nucleares/genética
Fenótipo
Fosfoproteínas Fosfatases/genética
Proteínas Proto-Oncogênicas c-kit/metabolismo
Rodamina 123/metabolismo
Tetraspanina 30/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCB5 protein, human); 0 (ATP-Binding Cassette, Sub-Family B, Member 1); 0 (Antigens, Neoplasm); 0 (Antineoplastic Agents, Alkylating); 0 (CD24 Antigen); 0 (CD24 protein, human); 0 (CD44 protein, human); 0 (CD63 protein, human); 0 (Carbazoles); 0 (ENG protein, human); 0 (Endoglin); 0 (Fluorescent Dyes); 0 (GAGE1 protein, human); 0 (Glycosides); 0 (Hyaluronan Receptors); 0 (LCS1269); 0 (Neoplasm Proteins); 0 (Nuclear Proteins); 0 (PRAME protein, human); 0 (Tetraspanin 30); 0 (aranoza); 126547-89-5 (Intercellular Adhesion Molecule-1); 1N3CZ14C5O (Rhodamine 123); 684-93-5 (Methylnitrosourea); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 3.1.3.16 (CTDSP1 protein, human); EC 3.1.3.16 (Phosphoprotein Phosphatases)
[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:161025
[St] Status:MEDLINE
[do] DOI:10.1097/CMR.0000000000000308


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[PMID]:29192497
[Au] Autor:Liang Q; Chalamaiah M; Ren X; Ma H; Wu J
[Ad] Endereço:School of Food and Biological Engineering, Jiangsu University , 301 Xuefu Road, Zhenjiang, Jiangsu 212013, China.
[Ti] Título:Identification of New Anti-inflammatory Peptides from Zein Hydrolysate after Simulated Gastrointestinal Digestion and Transport in Caco-2 Cells.
[So] Source:J Agric Food Chem;66(5):1114-1120, 2018 Feb 07.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chronic inflammation is an underlying contributor to various chronic diseases. The objectives of this study were to investigate the anti-inflammatory activity of zein hydrolysate after simulated gastrointestinal digestion and Caco-2 cell absorption and to identify novel anti-inflammatory peptides after transport across Caco-2 cells. Three zein hydrolysates were prepared and further digested using gastrointestinal proteases; their transports were studied in Caco-2 cells. Anti-inflammatory activity was studied in endothelial EA.hy926 cells. Three zein hydrolysates and their digests significantly decreased the expression of tumor necrosis factor-α (TNF-α) induced pro-inflammatory vascular cell adhesion molecule-1 (VCAM-1) by 37.3-66.0%. Eleven novel peptides with 5-9 amino acid residues were sequenced; three peptides showed strong anti-inflammatory activity by inhibiting the VCAM-1 by 54-38.9% and intercellular cell adhesion molecule-1 (ICAM-1) by 36.5-28.6% at 0.2 mM. A new approach to identify novel anti-inflammatory peptides that could survive gastrointestinal digestion and absorption was developed.
[Mh] Termos MeSH primário: Anti-Inflamatórios/análise
Digestão
Trato Gastrointestinal/metabolismo
Peptídeos/análise
Zeína/química
[Mh] Termos MeSH secundário: Anti-Inflamatórios/farmacologia
Transporte Biológico
Células CACO-2
Linhagem Celular
Trato Gastrointestinal/enzimologia
Seres Humanos
Hidrólise
Molécula 1 de Adesão Intercelular/efeitos dos fármacos
Peptídeo Hidrolases/metabolismo
Peptídeos/metabolismo
Peptídeos/farmacologia
Fator de Necrose Tumoral alfa/antagonistas & inibidores
Molécula 1 de Adesão de Célula Vascular/antagonistas & inibidores
Zeína/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Peptides); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Cell Adhesion Molecule-1); 126547-89-5 (Intercellular Adhesion Molecule-1); 9010-66-6 (Zein); EC 3.4.- (Peptide Hydrolases)
[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:171202
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b04562


  4 / 16653 MEDLINE  
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[PMID]:28468674
[Au] Autor:Cunningham DA; Lin JW; Brugat T; Jarra W; Tumwine I; Kushinga G; Ramesar J; Franke-Fayard B; Langhorne J
[Ad] Endereço:The Francis Crick Institute, London, NW1 1AT, UK. Deirdre.Cunningham@crick.ac.uk.
[Ti] Título:ICAM-1 is a key receptor mediating cytoadherence and pathology in the Plasmodium chabaudi malaria model.
[So] Source:Malar J;16(1):185, 2017 05 03.
[Is] ISSN:1475-2875
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Parasite cytoadherence within the microvasculature of tissues and organs of infected individuals is implicated in the pathogenesis of several malaria syndromes. Multiple host receptors may mediate sequestration. The identity of the host receptor(s), or the parasite ligand(s) responsible for sequestration of Plasmodium species other than Plasmodium falciparum is largely unknown. The rodent malaria parasites may be useful to model interactions of parasite species, which lack the var genes with their respective hosts, as other multigene families are shared between the species. The role of the endothelial receptors ICAM-1 and CD36 in cytoadherence and in the development of pathology was investigated in a Plasmodium chabaudi infection in C57BL/6 mice lacking these receptors. The schizont membrane-associated cytoadherence (SMAC) protein of Plasmodium berghei has been shown to exhibit reduced CD36-associated cytoadherence in P. berghei ANKA-infected mice. METHODS: Parasite tissue sequestration and the development of acute stage pathology in P. chabaudi infections of mice lacking CD36 or ICAM-1, their respective wild type controls, and in infections with mutant P. chabaudi parasites lacking the smac gene were compared. Peripheral blood parasitaemia, red blood cell numbers and weight change were monitored throughout the courses of infection. Imaging of bioluminescent parasites in isolated tissues (spleen, lungs, liver, kidney and gut) was used to measure tissue parasite load. RESULTS: This study shows that neither the lack of CD36 nor the deletion of the smac gene from P. chabaudi significantly impacted on acute-stage pathology or parasite sequestration. By contrast, in the absence of ICAM-1, infected animals experience less anaemia and weight loss, reduced parasite accumulation in both spleen and liver and higher peripheral blood parasitaemia during acute stage malaria. The reduction in parasite tissue sequestration in infections of ICAM-1 null mice is maintained after mosquito transmission. CONCLUSIONS: These results indicate that ICAM-1-mediated cytoadherence is important in the P. chabaudi model of malaria and suggest that for rodent malarias, as for P. falciparum, there may be multiple host and parasite molecules involved in sequestration.
[Mh] Termos MeSH primário: Antígenos CD36/genética
Molécula 1 de Adesão Intercelular/genética
Malária/parasitologia
Plasmodium chabaudi/fisiologia
Proteínas de Protozoários/genética
[Mh] Termos MeSH secundário: Animais
Antígenos CD36/metabolismo
Feminino
Molécula 1 de Adesão Intercelular/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Plasmodium chabaudi/genética
Proteínas de Protozoários/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD36 Antigens); 0 (Icam1 protein, mouse); 0 (Protozoan Proteins); 126547-89-5 (Intercellular Adhesion Molecule-1)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1186/s12936-017-1834-8


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[PMID]:28456769
[Au] Autor:Al Dera H
[Ad] Endereço:Department of Basic Medical Sciences, College of Medicine at King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), Riyadh, Kingdom of Saudi Arabia. derah@ksau-hs.edu.sa.
[Ti] Título:Neuroprotective effect of resveratrol against late cerebral ischemia reperfusion induced oxidative stress damage involves upregulation of osteopontin and inhibition of interleukin-1beta.
[So] Source:J Physiol Pharmacol;68(1):47-56, 2017 Feb.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:This study was carried out to investigate the expression pattern and role of osteopontin (OPN) in late global ischemia-reperfusion (I/R) injury with or without resveratrol (RES) pre-treatment. Young male rats were divided into 3 groups (n = 12) of I) sham, II) I/R model group and III) I/R + RES. Vehicle and RES (20 mg/kg) were administered to designed groups intraperitoneally 30 days prior global I/R injury (2-VO) induction and continued for 7 days, later. Then, percentages of infarct areas, mRNA levels of OPN, inducible nitric oxide synthase (iNOS) and other biochemical parameter related to endogenous antioxidants activities and inflammation were measured in the cerebral cortices of all groups. Significant elevations in the levels of malondialdehyde (MDA), the inflammatory mediator interleukin 1ß (IL-1ß), chemokines (KC and MIP-2) and adhesive molecules (ICAM-1) as well as parallel reductions in enzymes activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and chloramphenicol acetyltransferase (CAT) were observed in the cerebral homogenates of rats with late I/R injury. Associated with these changes, mRNA levels of OPN were significantly downregulated and those of iNOS and Bax were upregulated. All these changes were reversed by in 2-VO I/R induced rats pre-administered RES. These findings suggest that inhibition of sustained inflammatory response driven by IL-1ß, decreased activities of endogenous antioxidants and downregulation of OPN induced upregulation of iNOS play important roles in the pathogenesis of neurodegeneration during late cerebral I/R injury, effects that can be modulated by RES which might explain its neuroprotection effect during late global ischemia.
[Mh] Termos MeSH primário: Isquemia Encefálica/metabolismo
Fármacos Neuroprotetores/farmacologia
Traumatismo por Reperfusão/metabolismo
Estilbenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Isquemia Encefálica/tratamento farmacológico
Catalase/metabolismo
Córtex Cerebral/metabolismo
Quimiocina CXCL2/metabolismo
Quimiocinas/metabolismo
Glutationa Peroxidase/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Interleucina-1beta/antagonistas & inibidores
Interleucina-1beta/metabolismo
Masculino
Fármacos Neuroprotetores/uso terapêutico
Óxido Nítrico Sintase Tipo II/genética
Osteopontina/genética
Estresse Oxidativo/efeitos dos fármacos
Ratos Wistar
Traumatismo por Reperfusão/tratamento farmacológico
Estilbenos/uso terapêutico
Superóxido Dismutase/metabolismo
Regulação para Cima
Proteína X Associada a bcl-2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bax protein, rat); 0 (Chemokine CXCL2); 0 (Chemokines); 0 (Cxcl2 protein, rat); 0 (IL1B protein, rat); 0 (Interleukin-1beta); 0 (Neuroprotective Agents); 0 (Spp1 protein, rat); 0 (Stilbenes); 0 (bcl-2-Associated X Protein); 106441-73-0 (Osteopontin); 126547-89-5 (Intercellular Adhesion Molecule-1); 147037-79-4 (keratinocyte-derived chemokines); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, rat); EC 1.15.1.1 (Superoxide Dismutase); Q369O8926L (resveratrol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:27771726
[Au] Autor:Obi AT; Andraska E; Kanthi Y; Luke CE; Elfline M; Madathilparambil S; Siahaan TJ; Jaffer FA; Wakefield TW; Raghavendran K; Henke PK
[Ad] Endereço:Conrad Jobst Vascular Research Laboratory, University of Michigan Medical School, Ann Arbor, Mich., USA.
[Ti] Título:Gram-Negative Pneumonia Alters Large-Vein Cell-Adhesion Molecule Profile and Potentiates Experimental Stasis Venous Thrombosis.
[So] Source:J Vasc Res;53(3-4):186-195, 2016.
[Is] ISSN:1423-0135
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Pneumonia is a significant risk factor for the development of venous thrombosis (VT). Cell-adhesion molecules (CAMs) are linked to the pathogenesis of both pneumonia and VT. We hypothesized that remote infection would confer a prothrombogenic milieu via systemic elevation of CAMs. METHODS: Lung injury was induced in wild-type (C57BL/6) mice by lung contusion or intratracheal inoculation with Klebsiella pneumoniae or saline controls. K. pneumoniae-treated mice and controls additionally underwent inferior vena cava (IVC) ligation to generate VT. RESULTS: Lung-contusion mice demonstrated no increase in E-selectin or P-selectin whereas mice infected with K. pneumoniae demonstrated increased circulating P-selectin, ICAM-1, VCAM-1 and thrombin-antithrombin (TAT) complexes. Mice with pneumonia formed VT 3 times larger than controls, demonstrated significantly more upregulation of vein-wall and systemic CAMs, and formed erythrocyte-rich thrombi. CONCLUSION: Elevated CAM expression was identified in mice with pneumonia, but not lung contusion, indicating that the type of inflammatory stimulus and the presence of infection drive the vein-wall response. Elevation of CAMs was associated with amplified VT and may represent an alternate mechanism by which to target the prevention of VT.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/sangue
Infecções por Klebsiella/complicações
Klebsiella pneumoniae/patogenicidade
Pneumonia Bacteriana/complicações
Veia Cava Inferior/metabolismo
Trombose Venosa/etiologia
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/sangue
Lesão Pulmonar Aguda/complicações
Animais
Antitrombina III
Moléculas de Adesão Celular/antagonistas & inibidores
Modelos Animais de Doenças
Fibrinolíticos/farmacologia
Molécula 1 de Adesão Intercelular/sangue
Infecções por Klebsiella/sangue
Infecções por Klebsiella/tratamento farmacológico
Infecções por Klebsiella/microbiologia
Ligadura
Masculino
Camundongos Endogâmicos C57BL
Selectina-P/sangue
Peptídeo Hidrolases/sangue
Pneumonia Bacteriana/sangue
Pneumonia Bacteriana/tratamento farmacológico
Pneumonia Bacteriana/microbiologia
Regulação para Cima
Molécula 1 de Adesão de Célula Vascular/sangue
Veia Cava Inferior/cirurgia
Trombose Venosa/sangue
Trombose Venosa/microbiologia
Trombose Venosa/prevenção & controle
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (Fibrinolytic Agents); 0 (Icam1 protein, mouse); 0 (P-Selectin); 0 (Vascular Cell Adhesion Molecule-1); 0 (antithrombin III-protease complex); 126547-89-5 (Intercellular Adhesion Molecule-1); 9000-94-6 (Antithrombin III); EC 3.4.- (Peptide Hydrolases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  7 / 16653 MEDLINE  
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[PMID]:29224353
[Au] Autor:Zhang S; Zou J; Li P; Zheng X; Feng D
[Ad] Endereço:Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Preventive Medicine, School of Public Health, Sun Yat-sen University , Guangzhou 510080, China.
[Ti] Título:Curcumin Protects against Atherosclerosis in Apolipoprotein E-Knockout Mice by Inhibiting Toll-like Receptor 4 Expression.
[So] Source:J Agric Food Chem;66(2):449-456, 2018 Jan 17.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Toll-like receptor 4 (TLR4) has been reported to play a critical role in the pathogenesis of atherosclerosis, the current study aimed to investigate whether curcumin suppresses atherosclerosis development in ApoE-knockout (ApoE ) mice by inhibiting TLR4 expression. ApoE mice were fed a high-fat diet supplemented with or without curcumin (0.1% w/w) for 16 weeks. Curcumin supplementation significantly reduced TLR4 expression and macrophage infiltration in atherosclerotic plaques. Curcumin also reduced aortic interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α), vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) expression, nuclear factor-κB (NF-κB) activity, and plasma IL-1ß, TNF-α, soluble VCAM-1 and ICAM-1 levels. In addition, aortic sinus sections revealed that curcumin treatment reduced the extent of atherosclerotic lesions and inhibited atherosclerosis development. In vitro, curcumin inhibited NF-κB activation in macrophages and reduced TLR4 expression induced by lipopolysaccharide. Our results indicate that curcumin protects against atherosclerosis at least partially by inhibiting TLR4 expression and its related inflammatory reaction.
[Mh] Termos MeSH primário: Apolipoproteínas E/deficiência
Aterosclerose/prevenção & controle
Curcumina/administração & dosagem
Receptor 4 Toll-Like/genética
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas E/genética
Aterosclerose/genética
Aterosclerose/metabolismo
Seres Humanos
Molécula 1 de Adesão Intercelular/genética
Molécula 1 de Adesão Intercelular/metabolismo
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Masculino
Camundongos
Camundongos Knockout
Receptor 4 Toll-Like/metabolismo
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Interleukin-1beta); 0 (Toll-Like Receptor 4); 0 (Tumor Necrosis Factor-alpha); 126547-89-5 (Intercellular Adhesion Molecule-1); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b04260


  8 / 16653 MEDLINE  
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[PMID]:29324806
[Au] Autor:Watanabe PDS; Trevizan AR; Silva-Filho SE; Góis MB; Garcia JL; Cuman RKN; Breithaupt-Faloppa AC; Sant Ana DMG; Nogueira de Melo GA
[Ad] Endereço:Biosciences and Physiopathology Program, Universidade Estadual de Maringá, Maringá, Paraná, Brazil.
[Ti] Título:Immunocompetent host develops mild intestinal inflammation in acute infection with Toxoplasma gondii.
[So] Source:PLoS One;13(1):e0190155, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Toxoplasma gondii (T. gondii) is the causative agent of toxoplasmosis, common zoonosis among vertebrates and high incidence worldwide. During the infection, the parasite needs to transpose the intestinal barrier to spread throughout the body, which may be a trigger for an inflammatory reaction. This work evaluated the inflammatory alterations of early T. gondii infection in peripheral blood cells, in the mesenteric microcirculation, and small intestinal tissue by measurement of MPO (myeloperoxidase) activity and NO (nitric oxide) level in rats. Animals were randomly assigned into control group (CG) that received saline orally and groups infected with 5,000 oocysts for 6 (G6), 12 (G12), 24 (G24), 48 (G48) and 72 hours (G72). Blood samples were collected for total and differential leukocyte count. Intravital microscopy was performed in the mesentery to evaluate rolling and adhesion of leukocytes. After euthanasia, 0.5cm of the duodenum, jejunum and ileum were collected for the determination of MPO activity, NO level and PCR to identify the parasite DNA and also the mesentery were collected to perform immunohistochemistry on frozen sections to quantify adhesion molecules ICAM-1, PECAM-1 and P-Selectin. The parasite DNA was identified in all infected groups and there was an increase in leukocytes in the peripheral blood and in expression of ICAM-1 and PECAM-1 in G6 and G12, however, the expression of P-selectin was reduced in G12. Leukocytes are in rolling process during the first 12 hours and they are adhered at 24 hours post-infection. The activity of MPO increased in the duodenum at 12 hours, and NO increased in the jejunum in G72 and ileum in G24, G48 and G72. Our study demonstrated that T. gondii initiates the infection precociously (at 6 hours) leading to a systemic activation of innate immune response resulting in mild inflammation in a less susceptible experimental model.
[Mh] Termos MeSH primário: Imunocompetência
Inflamação/patologia
Intestinos/patologia
Toxoplasma/patogenicidade
Toxoplasmose Animal/patologia
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Molécula 1 de Adesão Intercelular/metabolismo
Óxido Nítrico/metabolismo
Peroxidase/metabolismo
Ratos
Reação em Cadeia da Polimerase em Tempo Real
Toxoplasma/genética
Toxoplasma/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
126547-89-5 (Intercellular Adhesion Molecule-1); 31C4KY9ESH (Nitric Oxide); EC 1.11.1.7 (Peroxidase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190155


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[PMID]:29244817
[Au] Autor:Montiel-Dávalos A; Silva Sánchez GJ; Huerta-García E; Rueda-Romero C; Soca Chafre G; Mitre-Aguilar IB; Alfaro-Moreno E; Pedraza-Chaverri J; López-Marure R
[Ad] Endereço:Subdirección de Investigación Básica, Instituto Nacional de Cancerología, Ciudad de México, México.
[Ti] Título:Curcumin inhibits activation induced by urban particulate material or titanium dioxide nanoparticles in primary human endothelial cells.
[So] Source:PLoS One;12(12):e0188169, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Curcumin has protective effects against toxic agents and shows preventive properties for various diseases. Particulate material with an aerodynamic diameter of ≤10 µm (PM10) and titanium dioxide nanoparticles (TiO2-NPs) induce endothelial dysfunction and activation. We explored whether curcumin is able to attenuate different events related to endothelial activation. This includes adhesion, expression of adhesion molecules and oxidative stress induced by PM10 and TiO2-NPs. Human umbilical vein endothelial cells (HUVEC) were treated with 1, 10 and 100 µM curcumin for 1 h and then exposed to PM10 at 3 µg/cm2 or TiO2-NPs at 10 µg/cm2. Cell adhesion was evaluated by co-culture with U937 human myelomonocytic cells. Adhesion molecules expression was measured by flow cytometry after 3 or 24 h of exposure. Oxidative stress was determined by 2,7-dichlorodihydrofluorescein (H2DCF) oxidation. PM10 and TiO2-NPs induced the adhesion of U937 cells and the expression of E- and P-selectins, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and platelet-endothelial cell adhesion molecule-1 (PECAM-1). The expression of E- and P-selectins matched the adhesion of monocytes to HUVEC after 3 h. In HUVEC treated with 1 or 10 µM curcumin, the expression of adhesion molecules and monocytes adhesion was significantly diminished. Curcumin also partially reduced the H2DCF oxidation induced by PM10 and TiO2-NPs. Our results suggest an anti-inflammatory and antioxidant role by curcumin attenuating the activation caused on endothelial cells by exposure to particles. Therefore, curcumin could be useful in the treatment of diseases where an inflammatory process and endothelial activation are involved.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Curcumina/farmacologia
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Nanopartículas/toxicidade
Material Particulado/antagonistas & inibidores
[Mh] Termos MeSH secundário: Biomarcadores/metabolismo
Adesão Celular/efeitos dos fármacos
Cidades
Técnicas de Cocultura
Selectina E/genética
Selectina E/metabolismo
Fluoresceínas/química
Expressão Gênica
Células Endoteliais da Veia Umbilical Humana/citologia
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Molécula 1 de Adesão Intercelular/genética
Molécula 1 de Adesão Intercelular/metabolismo
México
Estresse Oxidativo/efeitos dos fármacos
Selectina-P/genética
Selectina-P/metabolismo
Material Particulado/farmacologia
Molécula-1 de Adesão Celular Endotelial de Plaquetas/genética
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Titânio/farmacologia
Células U937
Molécula 1 de Adesão de Célula Vascular/genética
Molécula 1 de Adesão de Célula Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Biomarkers); 0 (E-Selectin); 0 (Fluoresceins); 0 (ICAM1 protein, human); 0 (P-Selectin); 0 (Particulate Matter); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (SELE protein, human); 0 (Vascular Cell Adhesion Molecule-1); 106070-31-9 (2',7'-dichlorodihydrofluorescein); 126547-89-5 (Intercellular Adhesion Molecule-1); 15FIX9V2JP (titanium dioxide); D1JT611TNE (Titanium); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188169


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[PMID]:29183044
[Au] Autor:Blokhuis C; Doeleman S; Cohen S; Demirkaya N; Scherpbier HJ; Kootstra NA; Kuhle J; Teunissen CE; Verbraak FD; Pajkrt D
[Ad] Endereço:Department of Hematology, Immunology and Infectious Diseases, Emma Children's Hospital/Academic Medical Center, University of Amsterdam, The Netherlands.
[Ti] Título:Inflammatory and Neuronal Biomarkers Associated With Retinal Thinning in Pediatric HIV.
[So] Source:Invest Ophthalmol Vis Sci;58(13):5985-5992, 2017 Nov 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: The pathophysiology of neuroretinal thinning in children with human immunodeficiency virus (HIV) is poorly understood. The current study aimed to assess whether neuroretinal thinning in clinically stable perinatally HIV-infected children was associated with biomarkers of immune activation, inflammation, and neuronal damage. Methods: Inflammation-associated and neuronal damage markers were measured in blood and cerebrospinal fluid (CSF) of HIV-infected children aged 8 to 18 years. Using mixed-effects regression analyses, we assessed associations between these biomarkers and neuroretinal layer thickness, as measured with spectral-domain optical coherence tomography. Results: Thirty-two HIV-infected children (median age 13.6 years, 50% male) were included. Blood plasma levels of interleukin-6, monocyte chemoattractant protein-1, and soluble intercellular adhesion molecule-1 were inversely correlated with foveal inner plexiform layer thickness (coef = -4.40, P < 0.001; coef = -9.67, P = 0.047; coef = -10.48, P = 0.042, respectively). Plasma interleukin-6 was inversely correlated with foveal ganglion cell layer thickness (coef = -2.49, P = 0.010). Total Tau levels in CSF were inversely correlated with outer nuclear layer and inner segments thickness (foveal: coef = -19.3, P = 0.029; pericentral: coef = -18.09, P = 0.006) and pericentral total retinal thickness (coef = -28.2, P = 0.017). Conclusions: Neuroretinal thinning was associated with inflammation-associated and neuronal injury biomarkers in a cohort of antiretroviral therapy-treated perinatally HIV-infected children. These findings suggest that ongoing immune activation, inflammation, and neuronal injury occur in parallel with retinal thinning in pediatric HIV.
[Mh] Termos MeSH primário: Infecções por HIV/complicações
Retina/patologia
Degeneração Retiniana
[Mh] Termos MeSH secundário: Adolescente
Biomarcadores/sangue
Biomarcadores/líquido cefalorraquidiano
Quimiocina CCL2/sangue
Criança
Feminino
Seres Humanos
Molécula 1 de Adesão Intercelular/sangue
Interleucinas/sangue
Masculino
Análise de Regressão
Degeneração Retiniana/sangue
Degeneração Retiniana/líquido cefalorraquidiano
Degeneração Retiniana/patologia
Células Ganglionares da Retina/patologia
Tomografia de Coerência Óptica
Proteínas tau/líquido cefalorraquidiano
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Chemokine CCL2); 0 (Interleukins); 0 (tau Proteins); 126547-89-5 (Intercellular Adhesion Molecule-1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171201
[Lr] Data última revisão:
171201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22252



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