Chronic obstructive pulmonary disease (COPD) stands as a major contributor to mortality worldwide, with cigarette smoke being a primary causative factor. Acacetin has been reported to possess lung protective effects. However, the precise role and mechanism of Acacetin in COPD remains elusive. In this study, human bronchial epithelial cell line HBE135-E6E7 was treated with Acacetin under cigarette smoke extract (CSE) conditions. Cellular viability was assessed using CCK-8 and LDH kits. Reactive oxygen species (ROS) generation was tested with DCFH-DA staining. JC-1 staining was employed to examine the mitochondrial membrane potential (MMP). Additionally, hydroxynonenal (4-HNE) level was tested using immunofluorescence staining and mitochondrial lipid peroxidation was evaluated using MitoPeDPP staining. MitoSOX staining was used to detect mitochondrial (mito)-ROS. Fe level was measured using FerroOrange staining and the expression of ferroptosis-related proteins was detected with western blot. Besides, the binding between Acacetin and NRF2 was analyzed by molecular docking. The sequent NRF2 overexpression or knockdown was used to explore the regulation of Acacetin on NRF2/SLC7A11/GPX4 signaling. Results indicated that CSE significantly reduced the viability, augmented ROS generation and decreased MMP in HBE135-E6E7 cells, which were blocked by Acacetin addition. Moreover, Acacetin inhibited lipid peroxidation and ferroptosis in CSE-treated HBE135-E6E7 cells. Specifically, Acacetin targeted NRF2 and activated the NRF2/SLC7A11/GPX4 signaling in CSE-induced HBE135-E6E7 cells. Furthermore, NRF2 deficiency or ML-385 treatment notably restored the influences of Acacetin on oxidative stress and ferroptosis in HBE135-E6E7 cells challenged with CSE. In conclusion, Acacetin alleviated CSE-induced injury in HBE135-E6E7 cells by activating The NRF2/SLC7A11/GPX4 signaling to inhibit ferroptosis.
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