In the development of atherosclerosis, naringin has exhibited potential protective effects. However, the specific
mechanisms are not clearly understood. The aim of this trial was to determine the anti-oxidative and anti-inflammatory effects
of naringin and uncover the mechanisms in Tumor Necrosis Factor-alpha (TNF-α) induced Human Umbilical Vein
Endothelial Cells (HUVECs). Reactive Oxygen Species (ROS) were measured by flow cytometry assay. The levels of
NADPH oxidase 4 (Nox4), p22phox, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1
(VCAM-1) over-expressions were measured by qRT-PCR and Western blotting analyses. Activation of Phosphatidylinositol
3-kinase/Akt (PI3K/Akt) and Nuclear Factor-κB (NF-κB) was evaluated by Western blotting. Naringin inhibited
ROS production as well as over-expression levels of Nox4, p22phox induced by TNF-α. Naringin inhibited TNF-α induced
mRNA and protein over-expressions of ICAM-1 and VCAM-1. Naringin also suppressed activation of NF-κB and
PI3K/Akt signaling pathways. These results indicated the preventive effects of naringin on HUVECs injury caused by
oxidative stress and inflammation response and the effects might be obtained via inhibition of Nox4 and NF-κB pathways
as well as activation of PI3K/Akt pathway. Naringin may be useful in preventing endothelial dysfunction, therefore to
ameliorate the development of atherosclerosis.
Keywords: Inflammation, Nox4, naringin, oxidative stress, PI3K/Akt, HUVECs.
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