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Standardized Curcuminoids Extract (Curcuma longa L.) Protects against inflammation in Human Umbilical Vein Endothelial Cells (HUVEC)
Author(s) -
AngelMorales Gabriela,
Noratto Giuliana,
MertensTalcott Susanne
Publication year - 2009
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.23.1_supplement.899.4
Subject(s) - umbilical vein , curcumin , curcuminoid , viability assay , inflammation , curcuma , pharmacology , chemistry , tumor necrosis factor alpha , human umbilical vein endothelial cell , mtt assay , reactive oxygen species , vascular endothelial growth factor , endothelial stem cell , microbiology and biotechnology , biochemistry , apoptosis , in vitro , biology , medicine , immunology , traditional medicine , cancer research , vegf receptors
Vascular inflammation is suggested to play a key‐role in the initiation and progression of atherosclerosis. Turmeric, used as medicinal agent in India, contains polyphenolics known as curcuminoids, including curcumin, demethoxycurcumin, and bisdemethoxycurcumin. This study investigated the potential protective effects of standardized curcuminoid extract (SCE) against vascular inflammation induced by high glucose in human umbilical vein endothelial cells (HUVEC). SCE was characterized by HPLC‐PDA. In this study, high glucose (Glc) (25 mM) increased vascular cell adhesion‐1 (VCAM) interleukin (IL‐8), tumor necrosis factor (TNF) and nuclear factor kappa B (NF‐kB) expression up to 2.1, 1.9, 1.7 and 3.0 fold, respectively, compared to the control and treatment with SCE for 24 h inhibited their mRNA expression by up to 50, 70, 40 and 60%, respectively in a dose dependent manner (0‐25 mg/L), these effects were not due to decreased cell viability as assessed by the MTT test. SCE reversed Glc‐and lypopolysacharide (LPS) induced increase of microRNA 146a, the NF‐kB‐dependent gene up to levels found in control cells (6.25‐25 mg/L).In addition, treatment with SCE for 1h incubation at 25 and 50 mg/L blocked formation of Glc‐induced oxygen species (ROS) by 50 and 70% respectively. The present data suggest that SCE could suppress high glucose induced vascular inflammation generation of ROS in HUVEC. Grant Funding Source Texas A&M University