Taxifolin ameliorates cigarette smoke-induced chronic obstructive pulmonary disease via inhibiting inflammation and apoptosis

• DOI: 10.1016/j.intimp.2022.109577
• Publication Date: 2022-12-28T11:20:06Z
• Authors: Xiangming Liu; Yiming Ma; Lijuan Luo; Zihang Zeng; Dandan Zong; Yan Chen
• Keywords: Inflammation; Nicotiana; 0301 basic medicine; Mice; Pulmonary Disease, Chronic Obstructive; 0303 health sciences; 03 medical and health sciences; Humans; Animals; Apoptosis; Cigarette Smoking; 3. Good health

Chronic obstructive pulmonary disease (COPD) is a significant cause of morbidity and mortality worldwide and is characterized by chronic airway inflammation and lung parenchymal cell apoptosis. Cigarette smoke is the major risk factor for the occurrence and development of COPD. Taxifolin (TAX) showed promising pharmacological effects in the management of inflammation, oxidative stress, and apoptosis. In the present study, our results demonstrated that TAX significantly alleviated cigarette smoke-induced inflammation and apoptosis both in vivo and in vitro. TAX notably lowered the elevated total cell count in mouse BALF compared with that in the COPD group. The cigarette smoke-induced emphysematous changes were remarkably reversed by TAX. In addition, treatment with TAX suppressed the elevated mRNA and protein levels of IL-1β, IL-6 and TNF-α in COPD mouse lung tissue and cigarette smoke extract (CSE)-treated human bronchial epithelial cells (HBECs). Additionally, TAX significantly decreased the ratios of p-iκB to iκB and p-p65 to p65 compared with the COPD group and CSE-treated HBECs. Moreover, the results of the TUNEL assay and flow cytometry also demonstrated the anti-apoptotic effect of TAX in mouse lung tissue and HBECs. Furthermore, the elevated Bax and CCP3 levels and decreased Bcl-2 levels induced by cigarette smoke were significantly reversed by TAX treatment in vivo and in vitro. Our results highlight the ameliorating effects of TAX against cigarette smoke-induced inflammation and apoptosis in the pathogenesis of COPD.