ArticleInternational journal of molecular sciences2025
Non-Thermal Plasma Attenuates TNF-α-Induced Endothelial Inflammation via ROS Modulation and NF-κB Inhibition.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Characterization of the potential antihypertensive activity ofFood science and biotechnology · 2026Article
- CarbopolGels (Basel, Switzerland) · 2026Article
- Cellular responses to prolonged non-thermal plasma exposure in Schizosaccharomyces pombe.Applied microbiology and biotechnology · 2026Article
- Cold Atmospheric Plasma Promotes Anti-Inflammatory and Regenerative Responses in Oral Soft Tissue through Redox-Driven Mitochondrial Regulation.ACS omega · 2026Article
- SZC-6 Promotes Diabetic Wound Healing in Mice by Modulating the M1/M2 Macrophage Ratio and Inhibiting the MyD88/NF-χB Pathway.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Unveiling the anti-inflammatory potential of olive leaf phenolic extracts in diabetes-related endothelial dysfunction.Frontiers in endocrinology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
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.
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Registered trials
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