Non-Thermal Plasma Attenuates TNF-α-Induced Endothelial Inflammation via ROS Modulation and NF-κB Inhibition.

Abstract

Non-thermal plasma (NTP) has emerged as a promising therapeutic tool due to its anti-inflammatory properties; however, its molecular effects on vascular endothelial inflammation remain unclear. This study investigated the effects of NTP on tumor necrosis factor-alpha (TNF-α)-induced inflammation in human umbilical vein endothelial cells (HUVECs). NTP treatment significantly reduced intracellular reactive oxygen species (ROS) levels and downregulated the expression of adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), which are key markers of endothelial activation. In addition, NTP suppressed mRNA expression of pro-inflammatory cytokines, including TNF-α, interleukin-1 beta (IL-1β), and interleukin-6 (IL-6). Mechanistically, NTP inhibited the nuclear translocation of phosphorylated NF-κB p65, indicating attenuation of NF-κB signaling. These results demonstrate that NTP modulates inflammatory responses in endothelial cells by attenuating ROS generation and suppressing NF-κB-mediated signaling. Our findings suggest that NTP may serve as a potential therapeutic strategy for treating vascular inflammation and related pathologies.