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Article Open Access

Overexpression of Annexin A1 protects against benzo[a]pyrene‑induced bronchial epithelium injury

  • Authors:
    • Yanfei Cui
    • Shengya Yang
  • View Affiliations / Copyright

    Affiliations: Department of Tuberculosis, Hangzhou Red Cross Hospital/Zhejiang Chinese Medicine and Western Medicine Integrated Hospital, Hangzhou, Zhejiang 310003, P.R. China
    Copyright: © Cui et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 349-357
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    Published online on: May 9, 2018
       https://doi.org/10.3892/mmr.2018.8998
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Abstract

The incidence of asthma is increasing worldwide. Bronchial epithelium injury is common in asthma. The regulatory role of Annexin A1 (ANXA1) in bronchial epithelium injury is currently not well understood. The aim of the present study was to evaluate the role of ANXA1 on bronchial epithelium injury. The cell viability and levels of apoptosis were respectively tested by Cell Counting Kit‑8 and flow cytometry. Reactive oxygen species (ROS) content and the activity of oxidative indicators were assessed by commercial kits. Enzyme linked immunosorbent assay was performed to detect the activity of active caspase‑3. Reverse transcription‑quantitative polymerase chain reaction and western blot assays were used to determine the expression levels of the target factors. The results demonstrated that ANXA1 improved the viability of benzo[a]pyrene (Bap)‑treated bronchial epithelial cells. The Bap‑induced oxidative stress was mitigated by the reduction in ROS generation, and the regulation of the activity of superoxide dismutase, glutathione peroxidases, malondialdehyde and lactic dehydrogenase. In addition, apoptosis was decreased by ANXA1 via the reduction of the expression of B‑cell lymphoma 2 (Bcl‑2), and the increase in the expression of Bcl‑2‑associated X protein and cyclin D1. Furthermore, the expression of phosphatase and tensin homolog (PTEN) and focal adhesion kinase (FAK) was rescued and the phosphorylation of phosphatidylinositol 3‑kinase (PI3K)/protein kinase B (Akt) was depressed by ANXA1, when compared with the Bap group. SF1670 treatment reversed the anti‑apoptotic effect of ANXA1. In conclusion, the results highlighted the protective effects of ANXA1 on bronchial epithelium injury, which most likely occurred via the PTEN/FAK/PI3K/Akt signaling pathway. Thus, the present study contributes to a potential therapeutic strategy for asthma patients.
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Copy and paste a formatted citation
Spandidos Publications style
Cui Y and Yang S: Overexpression of Annexin A1 protects against benzo[a]pyrene‑induced bronchial epithelium injury. Mol Med Rep 18: 349-357, 2018.
APA
Cui, Y., & Yang, S. (2018). Overexpression of Annexin A1 protects against benzo[a]pyrene‑induced bronchial epithelium injury. Molecular Medicine Reports, 18, 349-357. https://doi.org/10.3892/mmr.2018.8998
MLA
Cui, Y., Yang, S."Overexpression of Annexin A1 protects against benzo[a]pyrene‑induced bronchial epithelium injury". Molecular Medicine Reports 18.1 (2018): 349-357.
Chicago
Cui, Y., Yang, S."Overexpression of Annexin A1 protects against benzo[a]pyrene‑induced bronchial epithelium injury". Molecular Medicine Reports 18, no. 1 (2018): 349-357. https://doi.org/10.3892/mmr.2018.8998
Copy and paste a formatted citation
x
Spandidos Publications style
Cui Y and Yang S: Overexpression of Annexin A1 protects against benzo[a]pyrene‑induced bronchial epithelium injury. Mol Med Rep 18: 349-357, 2018.
APA
Cui, Y., & Yang, S. (2018). Overexpression of Annexin A1 protects against benzo[a]pyrene‑induced bronchial epithelium injury. Molecular Medicine Reports, 18, 349-357. https://doi.org/10.3892/mmr.2018.8998
MLA
Cui, Y., Yang, S."Overexpression of Annexin A1 protects against benzo[a]pyrene‑induced bronchial epithelium injury". Molecular Medicine Reports 18.1 (2018): 349-357.
Chicago
Cui, Y., Yang, S."Overexpression of Annexin A1 protects against benzo[a]pyrene‑induced bronchial epithelium injury". Molecular Medicine Reports 18, no. 1 (2018): 349-357. https://doi.org/10.3892/mmr.2018.8998
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