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Updated: Feb 5, 2026

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation
Published on: December 9, 2021
Luteolin alleviates ox-LDL-induced endothelial cell inflammation, apoptosis and ferroptosis by inhibiting the
Biao Yang1, Hui Zhang2, Shi-Jie Fang1
1Department of Cardiovascular Medicine, Peking University Shougang Hospital, Beijing, China.
Background:
Luteolin has been shown to have inhibitory effects on many human diseases, including atherosclerosis (AS). However, the specific role and underlying molecular mechanisms of luteolin in the progression of AS need to be further elucidated.
Methods:
Oxidized-low density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cells (HUVECs) was used to construct AS models in vitro. Cell proliferation, inflammation, apoptosis and angiogenesis were examined by CCK8 assay, EdU assay, ELISA, flow cytometry, and tube formation assay. The mRNA and protein levels of arachidonate 12-lipoxygenase (ALOX12) and N-acetyltransferase 10 (NAT10) were tested by qRT-PCR and western blot. The regulation of NAT10 on ALOX12 was confirmed by ac4C-RIP assay, RIP assay and dual-luciferase reporter assay.
Results:
Luteolin promoted cell proliferation and angiogenesis, while inhibited ox-LDL-induced HUVECs inflammation, apoptosis and ferroptosis. Luteolin targeted ALOX12 to reduce its expression. ALOX12 overexpression reversed the inhibitory effect of luteolin on ox-LDL-induced HUVECs injury. NAT10 promoted the ac4C modification of ALOX12 to increase its expression. NAT10 knockdown alleviated ox-LDL-induced HUVECs injury by downregulating ALOX12, and the protective effect of luteolin against ox-LDL-induced HUVECs injury could also be reversed by NAT10 overexpression.
Conclusion:
Luteolin may inhibit ox-LDL-induced endothelial cell injury by suppressing NAT10-mediated the ac4C modification of ALOX12, thereby alleviating the progression of AS.
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