Anti-inflammatory effects of neferine on LPS-induced human endothelium <i>via</i> MAPK, and NF-κβ pathways.

Abstract

This study aimed to evaluate the anti-inflammatory mechanism of neferine, a bisbenzylisoquinoline alkaloid, on the lipopolysaccharide (LPS)-induced inflammation in Human Umbilical Endothelial Cells (HUVECs) and pulmonary aorta cells. Production of pro-inflammatory cytokines and nitric oxide (NO) was determined using Griess reaction in human endothelial cells. The levels of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and mitogen-activated protein kinases (MAPKs) were analyzed using real time PCR and western blotting. Neferine significantly prevented the NO, TNF-α, COX-2, iNOS, IL-1B, and other inflammatory mediators formation in increasing dose as compared to LPS-induced human endothelial cells. The expressions of NADPH oxidase subunits p22phox, p47phox, and gp91phox were increased in LPS-induced HUVECs but neferein was able to reverse the effect in a dose-dependent manner. The anti-inflammatory effects of neferine in LPS-induced endothelial cells are attributed through the modulation of MAPK and NF-κβ pathways. Collectively, these results suggest that neferine could be beneficial in the early treatment of atherosclerosis to prevent stroke and heart disease.