Calycosin Alleviates Injury in Airway Epithelial Cells Caused by PM 2.5 Exposure via Activation of AMPK Signalling

  • Evid Based Complement Alternat Med. 2021 May 4:2021:8885716. doi: 10.1155/2021/8885716.
Chunyan Wang  1 ,  Jingjing Luo  2 ,  Xiaoxue Bai  1 ,  Shucheng Hua  1 ,  Jing Jie  2 ,  Han Liu  2 ,  Jinying Gao  2 ,  Lei Song  2
Affiliations
  • 1. Cadre's Wards, the First Hospital of Jilin University, Changchun 130021, Jilin, China.
  • 2. Department of Respiratory Medicine, The First Hospital of Jilin University, Changchun 130021, Jilin, China.
PMID: 34055025 DOI: 10.1155/2021/8885716
Abstract

Methods: Phospho-AMP-activated protein kinase (p-AMPK) and AMP-activated protein kinase (AMPK) were detected by western blot. Immunofluorescence staining was used to validate changes in the levels of nuclear factor kappa B (NF-кB) p65 nuclear translocation. Mice were administered intraperitoneally with calycosin one hour before anaesthesia and endotracheal instillation of PM 2.5. The extent of lung injury was evaluated in the H&E-stained lung sections. Apoptotic cells were detected by TUNEL staining.

Results: Administration of calycosin was increased in PM 2.5-treated B2B cells in a dose-dependent manner in vitro. Fluorescence signals from anti-NF-кB p65 were increased in nuclei of cells pretreated with calycosin. The level of p-AMPK was increased by calycosin in vitro and in vivo. After pretreatment with compound C, the inhibitory effects of calycosin on cytotoxicity, levels of inflammatory cytokines and p-AMPK, and levels of NF-кB p65 nuclear translocation were not significantly decreased in vitro or in vivo.

Conclusions: Calycosin effectively decreased the release of inflammatory cytokines and alleviated injury caused by PM 2.5. These effects were mediated through activation of AMPK to suppress NF-κB signalling.

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