Related Experiment Video
Updated: Jan 10, 2026
Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
Published on: March 15, 2024
Salvianic acid A ameliorates ox-LDL-induced ferroptosis in vascular endothelial cells by regulating TFRC
1Department of Cardiology, The Second Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Insights
Salvianic acid A (SAA) protects against atherosclerosis (AS) by inhibiting ferroptosis in human aortic endothelial cells (HAECs). SAA treatment reversed ox-LDL-induced cell damage and regulated iron metabolism and oxidative stress markers.
Area of Science:
- Cardiovascular biology
- Cellular pathology
- Pharmacology
Background:
- Atherosclerosis (AS) is a chronic inflammatory disease linked to cardiovascular diseases.
- Endothelial cell dysfunction is a key feature of AS.
- Ferroptosis, an iron-dependent cell death, plays a role in AS pathogenesis.
Purpose of the Study:
- To investigate the effect of Salvianic acid A (SAA) on ferroptosis in human aortic endothelial cells (HAECs) under AS conditions.
- To elucidate the underlying mechanisms of SAA's action in an in vitro AS model.
Main Methods:
- Human aortic endothelial cells (HAECs) were treated with oxidized low-density lipoprotein (ox-LDL) to induce an AS model.
- Cell viability was assessed using CCK8 and PI staining.
- Ferroptosis markers including iron content, reactive oxygen species (ROS), and malondialdehyde were measured.
- Protein expression (RAS, GPX4) and transferrin receptor (TFRC) mRNA levels were analyzed via Western blotting and RT-qPCR.
Main Results:
- Ox-LDL exposure decreased HAEC viability, increased cell death, iron content, ROS, and malondialdehyde levels.
- Ox-LDL treatment reduced GPX4 expression and increased RAS protein levels.
- SAA treatment rescued cell viability and reversed the ox-LDL-induced ferroptosis markers.
- SAA administration decreased TFRC levels in ox-LDL-treated cells, and TFRC overexpression counteracted SAA's protective effects.
Conclusions:
- Salvianic acid A (SAA) ameliorates atherosclerosis by inhibiting ferroptosis in human aortic endothelial cells.
- SAA exerts its protective effects by modulating iron metabolism and oxidative stress, partly through the regulation of TFRC.
- These findings offer novel insights into the therapeutic potential of SAA for AS treatment.
Abstract:
Atherosclerosis (AS) is an inflammatory disease which can results in the development of various cardiovascular diseases. Salvianic acid A (SAA) has certain curative effect on AS. This study focused on the effect of SAA on ferroptosis in human aortic endothelial cells (HAECs) in AS. HAECs were exposed to oxidized low-density lipoprotein (ox-LDL) to construct an in vitro AS model. CCK8 and PI stain was used to detect cell viability. Iron content, reactive oxygen species (ROS) as well as malondialdehyde was measured to detect the occurrence of ferroptosis. Protein expression were detected by western blotting. Real-time quantitative polymerase chain reaction (RT-qPCR) was applied to determine transferrin receptor (TFRC) levels. ox-LDL exposed resulted in decreased cell viability, increased mortality, increased iron content, ROS and malondialdehyde levels, increased RAS protein expression and decreased GPX4 protein expression of HAECs. However, the appropriate concentration of SAA could rescue this result. Besides, in ox-LDL-treated cells, t ferroptosis expression regulatory protein TFRC was decreased after SAA treatment. Overexpression of TFRC reversed the rescue effect of SAA on ox-LDL-treated cells. This study demonstrates that SAA ameliorates AS by affecting ferroptosis, thus providing new insights into the mechanism of AS development.
