Naringin Inhibits TNF-α Induced Oxidative Stress and Inflammatory Response in HUVECs via Nox4/NF-κ B and PI3K/Akt Pathways

Author(s): Wenshuang Li, Changyuan Wang, Jinyong Peng, Jing Liang, Yue Jin, Qi Liu, Qiang Meng, Kexin Liu, Huijun Sun

Journal Name: Current Pharmaceutical Biotechnology

Volume 15 , Issue 12 , 2014

Become EABM
Become Reviewer


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.

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2014
Page: [1173 - 1182]
Pages: 10
DOI: 10.2174/1389201015666141111114442
Price: $65

Article Metrics

PDF: 44