Honokiol ameliorates cigarette smoke‐induced damage of airway epithelial cells via the SIRT3/SOD2 signalling pathway

Abstract

AbstractCigarette smoking can cause damage of airway epithelial cells and contribute to chronic obstructive pulmonary disease (COPD). Honokiol is originally isolated from Magnolia obovata with multiple biological activities. Here, we investigated the protective effects of honokiol on cigarette smoke extract (CSE)‐induced injury of BEAS‐2B cells. BEAS‐2B cells were treated with 300 mg/L CSE to construct an in vitro cell injury model, and cells were further treated with 2, 5 and 10 μM honokiol, then cell viability and LDH leakage were analysed by CCK‐8 and LDH assay kits, respectively. Apoptosis was detected by flow cytometry analysis. ELISA was used to measure the levels of tumour necrosis factor (TNF)‐ɑ, IL‐1β, IL‐6, IL‐8 and MCP‐1. The results showed that honokiol (0.5–20 μM) showed non‐toxic effects on BEAS‐2B cells. Treatment with honokiol (2, 5 and 10 μM) reduced CSE (300 mg/L)‐induced decrease in cell viability and apoptosis in BEAS‐2B cells. Honokiol also decreased CSE‐induced inflammation through inhibiting expression and secretion of inflammatory cytokines, such as TNF‐ɑ, IL‐1β, IL‐6, IL‐8 and MCP‐1. Moreover, honokiol repressed CSE‐induced reactive oxygen species (ROS) production, decrease of ATP content and mitochondrial biogenesis, as well as mitochondrial membrane potential. Mechanistically, honokiol promoted the expression of SIRT3 and its downstream target genes, which are critical regulators of mitochondrial function and oxidative stress. Silencing of SIRT3 reversed the protective effects of honokiol on CSE‐induced damage and mitochondrial dysfunction in BEAS‐2B cells. These results indicated that honokiol attenuated CSE‐induced damage of airway epithelial cells through regulating SIRT3/SOD2 signalling pathway.