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Turmeric curcuminoids (Curcuma longa L.) interacts with microRNAs in the regulation of inflammation on Human Umbilical Vein Endothelial Cells (HUVEC)
Author(s) -
AngelMorales Gabriela,
Noratto Giuliana,
MertensTalcott Susanne
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.924.5
Subject(s) - microrna , umbilical vein , tlr4 , inflammation , curcumin , chemistry , transfection , curcuma , pharmacology , microbiology and biotechnology , biology , immunology , medicine , gene , traditional medicine , biochemistry , in vitro
The anti‐inflammatory properties of turmeric have been well‐investigated; however, the involvement of miRNAs in anti‐inflammatory properties of natural compounds has not been much investigated yet. We studied the potential protective effects of standardized curcuminoid extract (SCE) against vascular inflammation induced by lipopolysacharide (LPS) in HUVEC and investigated underlying miRNA based mechanisms. We screened miRNAs widely express on endothelial cells (miRNA 146a, miRNA 130, miRNA 126a and miRNA 155). However, only miRNA 146 clearly responded to LPS and reversal of this effect by SCE (2.5 –20 mg/L) down to 0.4 fold. miRNA 146 might be in control of Toll‐like receptor through a negative loop feedback regulation of NFK‐B activation. We analyzed the effect of SCE on NFK‐B expression and depended genes within the TLR4‐pathway which are target of miRNA146. SCE decreased the expression of NFK‐B, TRAF, IRAK1 and TLR4 by 0.6, 3.5, 1.6, and 0.84‐fold respectively. When cells were transfected with the mimic of miRNA146, SCE reversed the mimic‐induced expression of miRNA146 by 3‐fold. This indicates that the anti‐inflammatory effects of SCE are at least in part be exerted through the decrease in miRNA 146. Overall, curcuminoids showed anti‐inflammatory properties in HUVEC where a decreased of miR‐146a expression was involved in the underlying anti‐inflammatory mechanism. Grant Funding Source : ASN