title: Effects of n-3 PUFA supplementation on plasma soluble adhesion molecules: a meta-analysis of randomized controlled trials.
abstract: BACKGROUND
  Previous studies indicate that oral supplementation with n-3 PUFA protects against atherosclerotic disease by inhibiting inflammatory processes, which underlie atherosclerosis and are reflected by the plasma concentrations of soluble adhesion molecules. However, consistent results were not obtained among studies.
  
  
  OBJECTIVE
  The objective was to assess the effects of n-3 PUFA supplementation on plasma concentrations of soluble adhesion molecules.
  
  
  METHODS
  We conducted a meta-analysis of randomized controlled trials identified from PubMed, Embase, the Cochrane Library, and reference lists of relevant articles and reviews.
  
  
  RESULTS
  Eighteen studies were included. n-3 PUFA supplementation reduced plasma concentrations of soluble intercellular adhesion molecule-1 [sICAM-1; weighted mean difference (WMD): -5.17; 95% CI: -10.07, -0.27; P = 0.04] but had no significant effects on soluble vascular cell adhesion molecule-1 (WMD: -5.90; 95% CI: -17.63, 5.84; P = 0.32), soluble P-selectin (WMD: -1.53; 95% CI: -4.33, 1.28; P = 0.29), or soluble E-selectin (WMD: 0.46; 95% CI: -1.54, 2.46; P = 0.65). Subgroup analysis stratified by the subjects' health status showed that n-3 PUFA supplementation reduced sICAM-1 concentrations in healthy subjects (WMD: -8.87; 95% CI: -15.20, -2.53; P = 0.006; heterogeneity test: I² = 0%, P = 0.76) and in subjects with dyslipidemia (WMD: -15.31; 95% CI: -26.82, -3.81; P = 0.009; heterogeneity test: I² = 26%, P = 0.26).
  
  
  CONCLUSIONS
  n-3 PUFA supplementation can reduce plasma concentrations of sICAM-1. The effect is identified in both healthy subjects and subjects with dyslipidemia, which supports the hypothesis that n-3 PUFA can be supplemented as a primary or secondary means for preventing the development as well as the progression of atherosclerosis.
authors.affiliation: Department of Cardiology, Bethune First Hospital of Jilin University, Changchun City, China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Yang
authors.forename: Na
authors.initials: N
authors.lastname: Lu
authors.forename: Dongmei
authors.initials: D
authors.lastname: Chen
authors.forename: Lin
authors.initials: L
authors.lastname: Meng
authors.forename: Yang
authors.initials: Y
authors.lastname: Zheng
authors.forename: Rutai
authors.initials: R
authors.lastname: Hui
mesh_terms: D000328:Adult; D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D050197:Atherosclerosis / Q000209:etiology / Q000517:prevention & control; D015415:Biomarkers / Q000097:blood; D019587:Dietary Supplements; D050171:Dyslipidemias / Q000097:blood / Q000178:diet therapy* / Q000276:immunology; D019040:E-Selectin / Q000097:blood; D015525:Fatty Acids, Omega-3 / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood* / Q000737:chemistry; D008297:Male; D019007:P-Selectin / Q000097:blood; D016032:Randomized Controlled Trials as Topic; D012995:Solubility; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood / Q000737:chemistry
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D015415:Biomarkers; D019040:E-Selectin; D015525:Fatty Acids, Omega-3; D019007:P-Selectin; C546936:SELE protein, human; C546937:SELP protein, human; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1