Background Increased level of low-density lipoprotein (LDL) is a well-established risk factor of atherogenesis. Cigarette smoking leads to endothelial dysfunction, an early event of atherogenesis.
Objective To investigate the effect of smoking and smoking cessation on the atherogenesis of LDL and possible differences of this effect between long-term smokers with and without CAD
Methods Human umbilical vascular endothelial cells (HUVECs) were treated with 50 and 100 μg/ml LDL isolated from long-term smokers with or without coronary artery disease (CAD), before and after smoking cessation. Functional changes of HUVECs were evaluated by measuring oxidative markers (MDA, LOX-1), NO, eNOS and inflammatory markers (TNF-α, IL-1β, MMP-9).
Results PlasmaLDL levels of long-term (>10 years) smokers were significantly higher than that of non-smokers (p < 0.05). Smoking modified LDL increased endothelial LOX-1 and MDA levels, the higher level of LDL leaded to significantly higher levels of LOX-1 and MDA (p < 0.05). And 90 days’cessation partially yet significantly reversed LOX-1 levels (p < 0.05) but not MDA levels. Smoking modified LDL increased endothelial IL-1β, TNF-αand MMP-9 levels (all p < 0.05), the higher level of LDL leaded to significantly higher levels of IL-1β, TNF-α and MMP-9 (all p < 0.05). And 90 days’ cessation partially yet significantly reversed IL-1β, TNF-α and MMP-9 levels (all p < 0.05). LDL isolated from long-term smokers with CAD before cessation resulted in higher levels of IL-1β but lower levels of TNF-αand MMP-9 (all p < 0.05) compared to LDL isolated from long-term smokers without CAD before cessation. Smoking modified LDL decreased endothelial eNOS and NO levels (all p < 0.05), the higher level of LDL leaded to significantly lower levels of eNOS and NO (all p < 0.05). And 90 days cessation significantly increased eNOS (p < 0.05) levels and trends to decrease NO levels.
Conclusion Long-term cigarettes smoking had significant pro-oxidative and pro-inflammatory effects on LDLparticles which could lead to endothelial dysfunction. The detrimental effects of smoking on LDL could be partially reversed by 90days’ smoking cessation.
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