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Fucoxanthin ameliorates oxidative injury and inflammation of human bronchial epithelial cells induced by cigarette smoke extract via the PPARγ/NF‑κB signaling pathway

  • Authors:
    • Shaolei Chen
    • Lin Zhu
    • Jun Li
  • View Affiliations

  • Published online on: December 14, 2022     https://doi.org/10.3892/etm.2022.11768
  • Article Number: 69
  • Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Chronic obstructive pulmonary disease (COPD) is a prevalent and long‑term airway disease. It has been reported that fucoxanthin (FX) exhibits anti‑inflammatory and antioxidant effects. However, the underlying mechanism of FX in COPD remains unknown. Therefore, to investigate the effect of FX on COPD, BEAS‑2B cells were treated with cigarette smoke extract (CSE). The viability of BEAS‑2B cells treated with increasing doses of FX was assessed by Cell Counting Kit‑8. Lactate dehydrogenase (LDH) levels were measured using a corresponding kit. In addition, ELISA was carried out to detect the content of TNF‑α, IL‑1β and IL‑6. Additionally, a TUNEL assay and western blot analysis were performed to assess the cell apoptosis rate. Furthermore, 2',7'‑dichlorodihydrofluorescein diacetate was used to measure reactive oxygen species levels, while the contents of oxidative stress‑associated indexes were determined using the corresponding kits. Bioinformatics analysis using the search tool for interactions of chemicals database predicted that peroxisome proliferator‑activated receptor γ (PPARγ) may be a target of FX. The binding capacity of FTX with PPARγ was confirmed by molecular docking. The protein expression levels of the PPARγ/NF‑κB signaling‑associated factors were detected by western blot analysis. Finally, the regulatory mechanism of FX in COPD was revealed following cell treatment with the PPARγ inhibitor, T0070907. The results demonstrated that FX enhanced CSE‑induced BEAS‑2B cell viability and attenuated CSE‑induced BEAS‑2B cell inflammation and oxidative damage, possibly via triggering PPARγ/NF‑κB signaling. Pre‑treatment of BEAS‑2B cells with the PPARγ inhibitor, T0070907, could reverse the protective effects of FX on CSE‑induced BEAS‑2B cells. Overall, the present study suggested that FX could ameliorate oxidative damage as well as inflammation in CSE‑treated human bronchial epithelial in patients with COPD via modulating the PPARγ/NF‑κB signaling pathway.
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January-2023
Volume 25 Issue 1

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Spandidos Publications style
Chen S, Zhu L and Li J: Fucoxanthin ameliorates oxidative injury and inflammation of human bronchial epithelial cells induced by cigarette smoke extract via the PPARγ/NF‑κB signaling pathway. Exp Ther Med 25: 69, 2023
APA
Chen, S., Zhu, L., & Li, J. (2023). Fucoxanthin ameliorates oxidative injury and inflammation of human bronchial epithelial cells induced by cigarette smoke extract via the PPARγ/NF‑κB signaling pathway. Experimental and Therapeutic Medicine, 25, 69. https://doi.org/10.3892/etm.2022.11768
MLA
Chen, S., Zhu, L., Li, J."Fucoxanthin ameliorates oxidative injury and inflammation of human bronchial epithelial cells induced by cigarette smoke extract via the PPARγ/NF‑κB signaling pathway". Experimental and Therapeutic Medicine 25.1 (2023): 69.
Chicago
Chen, S., Zhu, L., Li, J."Fucoxanthin ameliorates oxidative injury and inflammation of human bronchial epithelial cells induced by cigarette smoke extract via the PPARγ/NF‑κB signaling pathway". Experimental and Therapeutic Medicine 25, no. 1 (2023): 69. https://doi.org/10.3892/etm.2022.11768