Neferine suppresses vascular endothelial inflammation by inhibiting the NF-κB signaling pathway

Abstract

The vascular endothelium, as the interface between the blood and the surrounding tissues, plays a pivotal role in inflammation. Neferine, which was isolated from Lotus Plumule, has many biological roles, such as antifibrotic, antioxidative, anti-inflammatory, and antineoplastic activities. We demonstrated the role of neferine in the inhibition of pro-adhesion and pro-inflammatory responses of endothelial cells in vitro. We found that neferine could significantly inhibit the adhesion of Tohoku Hospital Pediatrics-1 (THP-1) cells to primary human umbilical vein endothelial cells (HUVECs). At the molecular level, neferine could significantly alleviate the interleukin 1β (IL-1β)-induced mRNA and protein expression of intercellular adhesion molecule 1 (ICAM1) and vascular cell adhesion molecule 1 (VCAM1). Our data showed that neferine suppressed nuclear factor-κB (NF-κB) nuclear translocation and inhibited the NF-κB-p65-induced transcriptional activity of ICAM1 and VCAM1. Therefore, we concluded that neferine suppressed the inflammatory response in endothelial cells in vitro, which could be mainly due to inhibition of NF-κB signaling activation. Moreover, we found that neferine alleviated LPS-induced acute inflammation injury in vivo. Thus, neferine may serve as an effective regulator during the pathogenesis of vascular inflammatory diseases.