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Effect of Src tyrosine kinase on a rat model of asthma

  • Authors:
    • Min Wu
    • Jingping Yang
    • Tao Liu
    • Pengfei Xuan
    • Baoying Bu
    • Xiyuan Xu
    • Rina Wu
  • View Affiliations / Copyright

    Affiliations: Department of Respiratory and Critical Medicine, The Third Affiliated Hospital of Inner Mongolia Medical University, Baotou, Inner Mongolia Autonomous Region 014010, P.R. China
    Copyright: © Wu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 172
    |
    Published online on: December 27, 2021
       https://doi.org/10.3892/etm.2021.11095
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Abstract

Src tyrosine kinase is a protein encoded by the Src gene. The present study aimed to determine the role of Src protein kinase in asthma using small interfering RNA (siRNA) technology. Several Src siRNAs were designed and the most effective siRNA pair was selected. A rat model of asthma was established using ovalbumin, and the rats were treated with Src siRNA, empty vector or phosphate‑buffered saline (PBS). A non‑asthmatic control group was also established. The rats were clinically observed and Src mRNA and protein levels were measured by reverse transcription‑quantitative PCR and western blot analysis, respectively. Pathological observation of the lung tissue, counting of white blood cells (WBCs) and eosinophils (EOSs) and analysis of the concentrations of IL‑5, IL‑33 and IFN‑γ in the bronchoalveolar lavage fluid were performed. The expression levels of Src mRNA in the control, PBS, empty vector and siRNA groups were 110±30.7x103, 253±55.4x103, 254±41.3x103 and 180±50.9x103, respectively. Histochemical analysis of the lung tissue of rats in the siRNA group exhibited a relatively complete lung structure and little damage to the alveolar cavity. Src protein expression and IL‑5, IL‑33 levels, WBC and EOS levels were positively correlated with Src mRNA expression, while the IFN‑γ concentration was negatively correlated with Src mRNA expression. These results indicate that Src knockdown inhibits the release of tracheal inflammatory factors and significantly alleviates asthma in rats. In conclusion, the present study utilized a gene transfer technique to interfere with the expression of Src in rats, which decreased the levels of IL‑5, IL‑33, WBCs and EOSs and increased the level of IFN‑γ; these changes effectively ameliorated the condition of the trachea in asthmatic rats.
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Copy and paste a formatted citation
Spandidos Publications style
Wu M, Yang J, Liu T, Xuan P, Bu B, Xu X and Wu R: Effect of Src tyrosine kinase on a rat model of asthma. Exp Ther Med 23: 172, 2022.
APA
Wu, M., Yang, J., Liu, T., Xuan, P., Bu, B., Xu, X., & Wu, R. (2022). Effect of Src tyrosine kinase on a rat model of asthma. Experimental and Therapeutic Medicine, 23, 172. https://doi.org/10.3892/etm.2021.11095
MLA
Wu, M., Yang, J., Liu, T., Xuan, P., Bu, B., Xu, X., Wu, R."Effect of Src tyrosine kinase on a rat model of asthma". Experimental and Therapeutic Medicine 23.2 (2022): 172.
Chicago
Wu, M., Yang, J., Liu, T., Xuan, P., Bu, B., Xu, X., Wu, R."Effect of Src tyrosine kinase on a rat model of asthma". Experimental and Therapeutic Medicine 23, no. 2 (2022): 172. https://doi.org/10.3892/etm.2021.11095
Copy and paste a formatted citation
x
Spandidos Publications style
Wu M, Yang J, Liu T, Xuan P, Bu B, Xu X and Wu R: Effect of Src tyrosine kinase on a rat model of asthma. Exp Ther Med 23: 172, 2022.
APA
Wu, M., Yang, J., Liu, T., Xuan, P., Bu, B., Xu, X., & Wu, R. (2022). Effect of Src tyrosine kinase on a rat model of asthma. Experimental and Therapeutic Medicine, 23, 172. https://doi.org/10.3892/etm.2021.11095
MLA
Wu, M., Yang, J., Liu, T., Xuan, P., Bu, B., Xu, X., Wu, R."Effect of Src tyrosine kinase on a rat model of asthma". Experimental and Therapeutic Medicine 23.2 (2022): 172.
Chicago
Wu, M., Yang, J., Liu, T., Xuan, P., Bu, B., Xu, X., Wu, R."Effect of Src tyrosine kinase on a rat model of asthma". Experimental and Therapeutic Medicine 23, no. 2 (2022): 172. https://doi.org/10.3892/etm.2021.11095
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