cardiology careers collections past issues search home
     

Right arrow Help viewing high resolution images
Right arrow Return to article

Please click here to obtain permission to reproduce this image.

Click on image to view larger version.


Figure 2


Figure 2 Inhibition of CXCL16 Induction by Anti-Inflammatory Drugs

Down-regulation of (A) CXCL16 mRNA (F = 19.4, p = 0.001) and (B) CXCL16 protein secretion (F = 71.9, p < 0.001) by aspirin (ASA) in human macrophages. Cells were pre-treated with aspirin for 2 h and then for 24 h with LPS (1 µg/ml). **p < 0.01, ***p < 0.001 by t test compared to LPS-induced CXCL16 levels. (C) Down-regulation of CXCL16 mRNA in human macrophages by the nuclear factor-kappa-B inhibitor SN50 (t test p = 0.002). Cells were pretreated with SN50 or control peptide at 100 µg/ml for 2 h, then for 24 h with LPS (1 µg/ml). (D) Induction of CXCL16 in human macrophages by adenovirus over-expression (24 h) of activated I-kappa-B kinase compared to control virus (*t test p = 0.03). Results of representative experiments with triplicate samples are expressed as mean ± (SEM). GFP = green fluorescent protein; other abbreviations as in Figure 1.





Right arrow Return to article

 
  cardiology careers collections past issues search home