Protective Effect of Bakuchiol Against Vascular Inflammation in Human Umbilical Vein Endothelial Cells
Background The vascular endothelium regulates vascular inflammatory responses essential for controlling cardiovascular disease-induced complications. Moreover, regulating intercellular adhesion molecule-1 (ICAM-1) expression in response to pro-inflammatory stimuli is critical for controlling cardiovascular inflammation. Although bakuchiol is an established natural anti-inflammatory agent, its effects on intravascular inflammation remain elusive. Purpose This study aimed to assess bakuchiol’s inhibitory effects on vascular inflammatory responses by inducing adhesion molecule expression using tumor necrosis factor-α (TNF-α). Materials and Methods Vascular inflammation was stimulated with TNF-α by culturing human primary endothelial cells (ECs). Nuclear factor kappa B (NF-κB) signaling and adhesion molecule expression due to TNF-α stimulation were confirmed by Western blotting. Results ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1) expression in human umbilical vein endothelial cells (HUVECs) were significantly increased by TNF-α but decreased by bakuchiol. Bakuchiol inhibited monocyte adhesion by suppressing TNF-α-induced adhesion molecule expression and reduced NF-κB p65 subunit acetylation and phosphorylation. Conclusion These results demonstrate the potential of bakuchiol in preventing TNF-α-induced vascular inflammation and cardiovascular diseases. Bakuchiol may be used to prevent and treat vascular diseases, including hypertension, systemic inflammation, and oxidative stress.
Authors
- Jinyoung Hur (ORCID: https://orcid.org/0000-0003-1292-9290)
- Ae Sin Lee (ORCID: https://orcid.org/0000-0003-2685-1826)
- Sang Yoon Choi (ORCID: https://orcid.org/0000-0001-8712-6877)
Institutions
- Korea Food Research Institute (KR)
Publication Details
- Journal
- Pharmacognosy Magazine
- Published
- 2025-07-14
- DOI
- https://doi.org/10.1177/09731296251355167
- Primary Topic
- Bioactive natural compounds
- Type
- article
- Field-Weighted Citation Impact
- 0.00