Anti-inflammatory function of apolipoprotein B-depleted plasma is impaired in non-alcoholic fatty liver disease

BackgroundNon-alcoholic fatty liver disease (NAFLD) is associated with an increased risk of cardiovascular events. HDL exerts various protective functions on the cardiovascular system including anti-inflammatory activity by suppressing adhesion molecules expression in inflammation-induced endothelial cells. This study was designed to search if the anti-inflammatory capacity of apolipoprotein B-depleted plasma (apoB-depleted plasma) is altered in NAFLD patients. MethodsA total of 83 subjects including 42 NAFLD and 41 control subjects were included in this cross-sectional study. Anti-inflammatory function of HDL was determined as the ability of apoB-depleted plasma to inhibit tumor necrosis factor-alpha (TNF-alpha)-induced expression of adhesion molecules in human umbilical vein endothelial cells (HUVECs). ResultsIncubation of inflammation-stimulated HUVECs with the NAFLD patients' apo-B depleted plasma led to higher levels of expression of adhesion molecules compared to the control subjects' plasma samples, reflecting an impaired anti-inflammatory capacity of apoB-depleted plasma in the NAFLD patients. Impaired anti-inflammatory capacity of apoB-depleted plasma was correlated with fatty liver and obesity indices. After adjustment with obesity indices, the association of anti-inflammatory capacity of apoB-depleted plasma with NAFLD remained significant. ConclusionImpaired anti-inflammatory activity of apoB-depleted plasma was independently associated with NAFLD.

Automated summary

The study found that impaired anti-inflammatory activity of apoB-depleted plasma was associated with NAFLD, as indicated by the lower ability to inhibit the expression of adhesion molecules in inflammation-induced endothelial cells. This association remained significant even after adjusting for obesity indices.