LuQi Formula attenuates Cardiomyocyte ferroptosis via activating Nrf2/GPX4 signaling axis in heart failure.

• DOI: 10.1016/j.phymed.2024.155357
• Publication Date: 2024-01-14T15:55:03Z
• Authors: Peipei Cheng; Xinting Wang; Qian Liu; Tianshu Yang; Enrui Dai; Wanjing Sha; Huiyan Qu; Hua Zhou

The terminal stage of all cardiovascular diseases typically culminates in heart failure (HF), with no effective intervention available to halt its progression. LuQi formula (LQF) has been employed clinical for numerous years significantly ameliorate cardiac function HF patients. Nevertheless, the underlying mechanism LQF's efficacy remains inadequately comprehended. Cardiomyocyte ferroptosis served as a pathogenic HF. goal current experiment was ascertain whether LQF ameliorates by preventing cardiomyocyte and elucidate intrinsic involved. This research objective is investigate impact attenuating failure. Transverse aortic constriction (TAC) performed construct mouse model. Neonatal rat cardiomyocytes (NRCMs) were subjected vitro experiments. High-performance liquid chromatography (HPLC) identified bioactive compounds LQF. Transcriptomic quantitative proteomic analyses revealed potential targets anti-HF. Specifically, histological staining evaluated hypertrophy fibrosis. Transmission electron microscopy (TEM) observed mitochondrial morphology. content Fe2+, ROS, MDA, GSH, GSSH detected using kits. Molecular docking binding activities between essential active ingredients critical proteins ferroptosis. Mechanistically, expression levels Nrf2, Keap1, HO-1, SLC7A11, GPX4 qPCR, Western blot (WB), or immunohistochemical staining. primary nine detected. demonstrated that may Histomorphometric attenuates myocardial TEM diminished shrinkage increased membrane density tissue. Additionally, reactive oxygen species (ROS) generation suppressed Furthermore, molecular technique had suitable GPX4, SLC7A11. analysis further verified activated Nrf2/GPX4 signaling axis. decreased SLC7A11 HO-1 expression. These results prevents via activating axis suppressing Concurrently, it contributed elucidating provided scientific rationale development novel therapeutic drug.