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High molecular weight hyaluronic acid inhibits advanced glycation endproduct‐induced NF‐κB activation and cytokine expression
Author(s) -
Neumann Arne,
Schinzel Reinhard,
Palm Dieter,
Riederer Peter,
Münch Gerald
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)00731-0
Subject(s) - hyaluronic acid , proinflammatory cytokine , glycation , chemistry , inflammation , tumor necrosis factor alpha , oxidative stress , nf κb , cytokine , transcription factor , interleukin 6 , biochemistry , microbiology and biotechnology , endocrinology , medicine , immunology , signal transduction , biology , receptor , gene , anatomy
Advanced glycation endproducts (AGEs), which accumulate on long‐lived proteins and protein deposits (amyloids), induce the expression of proinflammatory cytokines through NF‐κB‐dependent pathways. Hyaluronic acid with a molecular weight above 1.2 MDa (HMW‐HA) inhibits the AGE‐induced activation of the transcription factor NF‐κB and the NF‐κB‐regulated cytokines interleukin‐1α, interleukin‐6 and tumor necrosis factor‐α. Since the molecular weight of hyaluronic acid in humans decreases with age and under conditions of oxidative stress, it is likely that the protective effect of HMW‐HA against AGE‐induced cellular activation is lost at sites of chronic inflammation and in older age.