Premium
Inhibition of TNF‐α‐induced reactive oxygen species generation, cell Adhesion molecule expression and NF‐κB activation by 5‐hydroxymethylfurfural in human umbilical vein endothelial cells
Author(s) -
Kim Hye kyung,
Kim Hyo Jin,
Park Jin Kyeong,
Lee Eun Na,
Oh SaeOck,
Baek SunYong,
Kim BongSeon,
Choi YoungWhan,
Yoon Sik
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.956.5
Subject(s) - umbilical vein , tumor necrosis factor alpha , reactive oxygen species , chemistry , cell adhesion molecule , inflammation , endothelial activation , nf κb , cell adhesion , endothelial stem cell , biochemistry , microbiology and biotechnology , pharmacology , cancer research , cell , immunology , signal transduction , medicine , in vitro , biology
Inflammation plays a critical role in the pathogenesis and progression of atherosclerotic vascular disease. The current study explored if 5‐hydroxymethylfurfural (HMF) isolated from aged black garlic extract could attenuate the activities of adhesion molecules in tumor necrosis factor‐α (TNF‐α)‐stimulated human umbilical vein endothelial cells (HUVECs). The study was performed on HUVECs that were pretreated with HMF for 1 h and then treated with TNF‐α. HUVECs treated with HMF showed markedly suppressed TNF‐α‐induced of VCAM‐1 and ICAM‐1 mRNA expression. HMF treatment also significantly decreased cell surface and total protein expression of VCAM‐1 and ICAM‐1 in a concentration‐dependent manner. In addition, HMF suppressed TNF‐α‐induced production of reactive oxygen species (ROS). Furthermore, HMF significantly inhibited NF‐κB transcription factor activation in TNF‐α‐stimulated HUVECs. Based on these findings, HMF is proposed as an effective new anti‐inflammatory agent that may have a potential therapeutic use for the prevention and treatment of vascular diseases such as atherosclerosis.