AI Article Synopsis
- A new study discovered that berberine (BBR) can inhibit the protein ACSL4, which is linked to cell damage through ferroptosis, and this could help protect against atherosclerosis.
- Researchers created a mouse model with a high-fat diet to simulate atherosclerosis and tested the effects of BBR on both this model and human endothelial cells damaged by oxidized low-density lipoprotein (ox-LDL).
- Findings showed that BBR not only inhibits ferroptosis associated with ACSL4 but also reduces lipid buildup and plaque formation, suggesting it could be a promising treatment strategy for atherosclerosis.
Article Abstract
The discovery of an inhibitor for acyl-CoA synthetase long-chain family member 4 (ACSL4), a protein involved in the process of cell injury through ferroptosis, has the potential to ameliorate cell damage. In this study, we aimed to investigate the potential of berberine (BBR) as an inhibitor of ACSL4 in order to suppress endothelial ferroptosis and provide protection against atherosclerosis. An atherosclerosis model was created in ApoE mice by feeding a high fat diet for 16 weeks. Additionally, a mouse model with endothelium-specific overexpression of ACSL4 was established. BBR was administered orally to assess its potential therapeutic effects on atherosclerosis. Human umbilical vein endothelial cells (HUVECs) were exposed to oxidized low density lipoprotein (ox-LDL) to simulate atherosclerotic endothelial damage in vitro. The interaction between ACSL4 and BBR has been confirmed, with BBR playing a role in inhibiting erastin-induced ferroptosis by regulating ACSL4. Additionally, BBR has been found to inhibit lipid deposition, plaque formation, and collagen deposition in the aorta, thereby delaying the progression of atherosclerosis. It also restored the abnormal expression of ferroptosis-related proteins in atherosclerotic vascular endothelial cells both in vivo and in vitro. In conclusion, BBR, acting as an ACSL4 inhibitor, can improve atherosclerosis by inhibiting ferroptosis in endothelial cells. This highlights the potential of targeted inhibition of vascular endothelial ACSL4 as a strategy for treating atherosclerosis, with BBR being a candidate for this purpose.
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| http://dx.doi.org/10.1016/j.biopha.2024.117081 | DOI Listing |
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