Sulforaphane reduces advanced glycation end products (AGEs)-induced inflammation in endothelial cells and rat aorta

Nutrition, Metabolism and Cardiovascular Diseases

Volumn 26, Issue 9, 2016, Pages 797-807

  Matsui, T ^a   Nakamura, N ^a   Ojima, A ^a   Nishino, Y ^a   Yamagishi, S I ^a  

^a KURUME UNIVERSITY SCHOOL OF MEDICINE   (Japan)

Author keywords

AGEs; Atherosclerosis; Oxidative stress; RAGE; Sulforaphane

Indexed keywords

ADVANCED GLYCATION END PRODUCT; ALANINE AMINOTRANSFERASE; ASPARTATE AMINOTRANSFERASE; CHOLESTEROL; GLUCOSE; HIGH DENSITY LIPOPROTEIN CHOLESTEROL; IMMUNOGLOBULIN G; INSULIN; INTERCELLULAR ADHESION MOLECULE 1; MONOCYTE CHEMOTACTIC PROTEIN 1; NITRATE REDUCTASE (NADPH); NITROGEN; REACTIVE OXYGEN METABOLITE; SULFORAPHANE; TRIACYLGLYCEROL; UREA; VASCULAR CELL ADHESION MOLECULE 1; ADVANCED GLYCATION END PRODUCT RECEPTOR; AGER PROTEIN, HUMAN; AGER PROTEIN, RAT; ANTIINFLAMMATORY AGENT; ANTIOXIDANT; AUTACOID; CELL ADHESION MOLECULE; ISOTHIOCYANIC ACID DERIVATIVE; MESSENGER RNA; SULFORAFAN;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; AORTIC ENDOTHELIAL CELL; ARTICLE; BIOCHEMISTRY; BLOOD VESSEL INJURY; COLUMN CHROMATOGRAPHY; ENZYME ACTIVITY; ENZYME LINKED IMMUNOSORBENT ASSAY; GENE EXPRESSION; HUMAN; HUMAN CELL; IMMUNOHISTOCHEMISTRY; INFLAMMATION; MALE; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; RAT; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; UMBILICAL VEIN ENDOTHELIAL CELL; ANIMAL; AORTA; AORTITIS; CHEMICALLY INDUCED; DISEASE MODEL; DOSE RESPONSE; DRUG EFFECTS; ENDOTHELIUM CELL; GENETICS; METABOLISM; TIME FACTOR; TUMOR CELL LINE; WISTAR RAT;

ADVANCED GLYCOSYLATION END PRODUCT-SPECIFIC RECEPTOR; ANIMALS; ANTI-INFLAMMATORY AGENTS; ANTIOXIDANTS; AORTA; AORTITIS; CELL ADHESION MOLECULES; CELL LINE, TUMOR; DISEASE MODELS, ANIMAL; DOSE-RESPONSE RELATIONSHIP, DRUG; ENDOTHELIAL CELLS; GLYCOSYLATION END PRODUCTS, ADVANCED; HUMAN UMBILICAL VEIN ENDOTHELIAL CELLS; INFLAMMATION MEDIATORS; ISOTHIOCYANATES; MALE; RATS, WISTAR; RNA, MESSENGER; TIME FACTORS;

EID: 84969523089     PISSN: 09394753     EISSN: 15903729     Source Type: Journal    
DOI: 10.1016/j.numecd.2016.04.008     Document Type: Article

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