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Article

The transfection of A20 gene prevents kidney from ischemia reperfusion injury in rats

  • Authors:
    • Lixin Wei
    • Xianghui Zhang
    • Qiuping Ye
    • Yueer Yang
    • Xiaowen Chen
  • View Affiliations / Copyright

    Affiliations: Department of Nephropathy, Union Hospital, Fujian Medical University, Fuzhou, Fujian 350001, P.R. China, Department of Nephropathy, The Fifth Affiliated Hospital of Zunyi Medical University, Zhuhai, Guangdong 519000, P.R. China
  • Pages: 1486-1492
    |
    Published online on: June 8, 2017
       https://doi.org/10.3892/mmr.2017.6725
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Abstract

Ischemia/reperfusion may induce inflammation and cell death through the nuclear factor (NF)‑κB signaling pathway. As a negative regulator of NF‑κB, zinc finger A20 exhibits anti-apoptotic and anti‑inflammatory effects in vitro. The present study was designed to upregulate A20 expression using an A20 transfection approach to investigate the in vivo protective effects of the A20 gene on renal ischemia reperfusion injury. The A20 gene was cloned into a pcDNA3.1 vector to construct the expression plasmid pcDNA3.1‑A20. The plasmid was wrapped with a liposome and injected intravenously into rats 48 h prior to establishing the models of renal ischemia reperfusion injury. Saline and the empty plasmid pcDNA3.1 were used as controls. Following 24 h post‑operation, A20 expression was determined using reverse transcription‑quantitative polymerase chain reaction and western blotting. The renal function and structure were assessed by analyzing the concentrations of serum creatinine (Scr), blood urea nitrogen (BUN) and histological features. Renal tissues were additionally examined for renal tubular cell apoptosis and NF‑κB activity. The results demonstrated that in vivo transfection of pcDNA3.1‑A20 induced renal A20 expression in rats. A20 overexpression in vivo significantly reduced renal injury as demonstrated by the improved levels of Scr and BUN and the reduction in histological damage. These improvements were accompanied by a suppression of renal proximal tubular epithelial cell apoptosis and an inhibition of NF‑κB activity. These results indicated that transfection of the A20 gene upregulates the expression of A20 in vivo and protects the kidneys from ischemia reperfusion injury via inhibition of the NF‑κB signal transduction pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Wei L, Zhang X, Ye Q, Yang Y and Chen X: The transfection of A20 gene prevents kidney from ischemia reperfusion injury in rats. Mol Med Rep 16: 1486-1492, 2017.
APA
Wei, L., Zhang, X., Ye, Q., Yang, Y., & Chen, X. (2017). The transfection of A20 gene prevents kidney from ischemia reperfusion injury in rats. Molecular Medicine Reports, 16, 1486-1492. https://doi.org/10.3892/mmr.2017.6725
MLA
Wei, L., Zhang, X., Ye, Q., Yang, Y., Chen, X."The transfection of A20 gene prevents kidney from ischemia reperfusion injury in rats". Molecular Medicine Reports 16.2 (2017): 1486-1492.
Chicago
Wei, L., Zhang, X., Ye, Q., Yang, Y., Chen, X."The transfection of A20 gene prevents kidney from ischemia reperfusion injury in rats". Molecular Medicine Reports 16, no. 2 (2017): 1486-1492. https://doi.org/10.3892/mmr.2017.6725
Copy and paste a formatted citation
x
Spandidos Publications style
Wei L, Zhang X, Ye Q, Yang Y and Chen X: The transfection of A20 gene prevents kidney from ischemia reperfusion injury in rats. Mol Med Rep 16: 1486-1492, 2017.
APA
Wei, L., Zhang, X., Ye, Q., Yang, Y., & Chen, X. (2017). The transfection of A20 gene prevents kidney from ischemia reperfusion injury in rats. Molecular Medicine Reports, 16, 1486-1492. https://doi.org/10.3892/mmr.2017.6725
MLA
Wei, L., Zhang, X., Ye, Q., Yang, Y., Chen, X."The transfection of A20 gene prevents kidney from ischemia reperfusion injury in rats". Molecular Medicine Reports 16.2 (2017): 1486-1492.
Chicago
Wei, L., Zhang, X., Ye, Q., Yang, Y., Chen, X."The transfection of A20 gene prevents kidney from ischemia reperfusion injury in rats". Molecular Medicine Reports 16, no. 2 (2017): 1486-1492. https://doi.org/10.3892/mmr.2017.6725
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