Decursin alleviates LPS-induced lung epithelial cell injury by inhibiting NF-κB pathway activation

• Jiangfeng Zhu ^[1] ; Xiaoping Dong ^[1]
  1. [1] General Medicine Ward, The First People’s Hospital of Fuyang Hangzhou, Hangzhou, Zhejiang Province, China.
• Localización: Allergologia et immunopathologia: International journal for clinical and investigate allergology and clinical immunology, ISSN-e 1578-1267, ISSN 0301-0546, Vol. 51, Nº. 1, 2023, págs. 37-43
• Idioma: inglés
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• Resumen

  • Objective: To reveal the possible effects of decursin on viability, oxidative stress, and inflammatory response in lipopolysaccharide (LPS)-treated human bronchial epithelial cells-2B (BEAS-2B) and human pulmonary artery endothelial cells (HPAEC) cells, and revealed the potential mechanisms.

    Methods: LPS was used to induce acute lung injury (ALI) in normal human lung epithelial cells, including BEAS-2B and HPAEC cells. Cell viability and apoptosis in response to LPS and decursin in BEAS-2B and HPAEC cells were, respectively, evaluated by MTT colorimetric and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays. The oxidative stress and inflammatory response in LPS-treated BEAS-2B and HPAEC cells were detected by enzyme-linked-immunosorbent serologic assay. In addition, the role of decursin in nuclear-factor-kappa B (NF-κB) activation was analyzed by immunoblot and immunofluorescence assays.

    Results: Our data revealed that decursin could alleviate the viability of LPS-induced BEAS-2B and HPAEC cells. Decursin could also reduce LPS-induced oxidative stress in BEAS-2B and HPAEC cells. In addition, it could reduce LPS-induced inflammation in BEAS-2B and HPAEC cells. Mechanically, decursin suppressed the activation of NF-κB pathway.

    Conclusion: Decursin suppressed NF-κB pathway, and therefore alleviated ALI.