Anti-inflammatory effects of high-density lipoprotein via regulation of nitric oxide synthase expression and Nf-κb transcription in activated human endothelial cells

• Published in: Pertanika Journal of Science and Technology
• Main Author: Wan Yusoff W.N.; Chua Y.-A.; Froemming G.R.A.; Ali A.M.; Nawawi H.
• Format: Article
• Language: English
• Published: Universiti Putra Malaysia Press 2017
• Online Access: https://www.scopus.com/inward/record.uri?eid=2-s2.0-85049124079&partnerID=40&md5=f0c7a66cc44b27132f891149f85fcd1a

Oxidation of low-density lipoprotein (LDL) and activation of the transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) are critical for the inflammatory response for endothelial dysfunction. The objective of this study is to investigate the effects of various doses of HDL on: (a) LDL susceptibility to oxidation; (b) expression of eNOS; and (c) expression of NF-κB p50 and p65. Different concentrations of HDL were incubated in LDL. The reaction rates of LDL susceptibility to oxidation were obtained by kinetic modeling analysis. For determination of eNOS, NF-κB p50 and p65 expression, different HDL concentrations were incubated in lipo polysacharides (LPS)-stimulated human umbilical vein endothelial cell line for 16 hours. Protein was extracted and analysed by western blot and nuclear transcription factor, for example, Co-incubation of LDL with increasing HDL concentrations showed longer lag time and lower reaction rate in a dose-dependent manner compared to controls (p<0.05). The eNOS expression at higher HDL concentration was significantly increased when compared to controls (p<0.05). HDL significantly decreased the expression of NF-κB p65 but not that of NF-κB p50. HDL protects LDL from oxidation, up regulates eNOS expression and down regulates the expression of NF-κB p65. These in part contribute to the role of HDL in the prevention and retardation of atherogenesis and atherosclerosis-related complications. © 2017 Universiti Putra Malaysia Press.