β-elemene inhibits monocyte-endothelial cells interactions via reactive oxygen species/MAPK/NF-κB signaling pathway...

Area of Science:

• Cardiovascular Research
• Pharmacology
• Cell Biology

Background:

• Monocyte recruitment to endothelial cells is crucial in early atherosclerosis.
• Beta-elemene shows potential in preventing atherosclerosis, but its mechanism is unclear.
• Understanding these interactions is key for developing new therapeutic strategies.

Purpose of the Study:

• To investigate the effects of beta-elemene on monocyte-endothelial cell interactions in atherosclerosis initiation.
• To elucidate the molecular mechanisms behind beta-elemene's anti-atherosclerotic effects in vitro.
• To provide pharmacological evidence for beta-elemene as a potential therapeutic agent.

Main Methods:

• Utilized in vitro models with human umbilical vein endothelial cells (HUVECs) and monocytes.
• Assessed HUVEC protection against hydrogen peroxide-induced injury.
• Measured monocyte adhesion and transendothelial migration.
• Investigated the role of nuclear factor-kappa B (NF-κB) and cell adhesion molecules.
• Analyzed reactive oxygen species (ROS) generation and mitogen-activated protein kinase (MAPK) signaling pathway activation.

Main Results:

• Beta-elemene protected HUVECs from oxidative stress.
• It inhibited monocyte adhesion and migration across inflamed endothelium.
• Suppression of NF-κB-dependent cell adhesion molecule expression was observed.
• Beta-elemene reduced ROS generation and prevented MAPK pathway activation in HUVECs.

Conclusions:

• Beta-elemene demonstrates protective effects against endothelial cell injury and monocyte infiltration.
• It acts by suppressing inflammatory signaling pathways, including NF-κB and MAPK.
• These findings support beta-elemene's potential as a therapeutic agent for atherosclerosis.