Isobavachalcone attenuates TNF-α-induced ICAM-1 and VCAM-1 expression in human umbilical vein endothelial cells by regulating the NF-κB signaling pathway

Vascular inflammation activated by pro-inflammatory cytokines is an inflammatory response that occurs in the early stages of atherosclerosis. Endothelial dysfunction in vascular inflammation begins with the expression of cell surface adhesion molecules by pro-inflammatory cytokines. The purpose of t...

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Bibliographic Details
Published in:Applied biological chemistry 2022, 65(4), , pp.1-6
Main Authors: Lee, Ae Sin, Hur, Jinyoung, Choi, Sang Yoon
Format: Article
Language:English
Subjects:
Adhesion
Applied Microbiology
Arteriosclerosis
Atherosclerosis
Biological Techniques
Bioorganic Chemistry
Cell adhesion
Cell adhesion molecules
Cell surface
Chemistry
Chemistry and Materials Science
Cytokines
Endothelial cells
Inflammation
Inflammatory response
Intercellular adhesion molecule 1
Monocytes
NF-κB protein
Phosphorylation
Signal transduction
Tumor necrosis factor-TNF
Tumor necrosis factor-α
Umbilical vein
Vascular cell adhesion molecule 1
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Summary:Vascular inflammation activated by pro-inflammatory cytokines is an inflammatory response that occurs in the early stages of atherosclerosis. Endothelial dysfunction in vascular inflammation begins with the expression of cell surface adhesion molecules by pro-inflammatory cytokines. The purpose of this study was to evaluate and verify the vascular inflammatory effects of isobavachalcone. In this study, we investigated the effects of isobavachalcone on inflammatory responses in vascular inflammation induced by the tumor necrosis factor-α (TNF-α) in human umbilical vein endothelial cells (HUVECs). TNF-α stimulation significantly increased the expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) proteins, and concentration-dependently decreased by isobavachalcone in HUVECs. Isobavachalcone suppressed TNF-α-induced ICAM-1 and VCAM-1 expression in HUVECs, thereby inhibiting TNF-α-induced increase in monocyte adhesion. In addition, isobavachalcone decreased the phosphorylation of the NF-κB (necrosis factor κB) p65 subunit. The findings of this study demonstrate that isobavachalcone prevents TNF-α-induced vascular inflammation and has the potential to protect against the early progression of atherosclerosis.
ISSN:2468-0834
2468-0842
DOI:10.1186/s13765-022-00717-7