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

Abstract

Objective: To reveal the possible effects of decursin on viability, oxidative stress, and inflam-matory 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-ĸB) 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.

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“…However, whether LTE can inhibit lung inflammation or other biological pathways to alleviate ALI through its active component Lut has not been fully covered. Furthermore, studies have shown that Decursin could mitigate LPS-evoked BEAS-2B and HPAEC cell injury via inactivating NF-κB pathway [ 15 ], and Chikusetsusaponin V could protect against LPS-stimulated ALI in mice by restraining NF-κB pathway activation [ 16 ]. However, whether the function of LTE in LPS-evoked ALI was concerned with NF-κB pathway remained unclear.…”