Luteolin target HSPB1 regulates endothelial cell ferroptosis to protect against radiation vascular injury

• DOI: 10.1371/journal.pone.0311922
• Publication Date: 2024-10-11T17:31:58Z
• Authors: Li Wen; Weiyuan Zhang; Jia Hu; Tao Chen; Yiming Wang; Changchang Lv; Min Li; Lisheng Wang; Fengjun Xiao
• Keywords: Male; Superoxide Dismutase; HSP27 Heat-Shock Proteins; Vascular System Injuries; Antioxidants; Mice; Human Umbilical Vein Endothelial Cells; Ferroptosis; Humans; Animals; Luteolin; Radiation Injuries; Heat-Shock Proteins; Research Article; Molecular Chaperones

Vascular endothelial damage due to ionizing radiation is the main pathological process of injury and cause various organs in nuclear accidents. Ferroptosis plays an important role radiation-induced cell death. We have previously reported that luteolin highly resistant ferroptosis. In present study, body weight, microvessel count, H&E, Masson staining results showed rescued radial vascular vivo . Cell Counting Kit 8 (CCK8), Giemsa clarified anti-ferroptosis ability with low toxicity. Malondialdehyde (MDA), superoxide dismutase (SOD), NADP + /NADPH, Fe 2+ staining, dihydroethidium (DHE) MitoTracker assays for ferroptosis-related metrics, we found enhances human umbilical vein cells (HUVECs) antioxidant capacity. Drug affinity responsive target stability (DARTS), surface plasmon resonance (SPR), computer simulated docking western blot heat shock protein beta-1 (HSPB1) one targets action. Luteolin inhibits ferroptosis by promoting expression HSPB1/solute carrier family 7 member 11 (SLC7A11)/ glutathione peroxidase 4 (GPX4). conclusion, preliminarily elucidated action provide a theoretical basis application diseases.