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Article

Role of TLR4/MyD88/NF‑κB signaling in the contrast‑induced injury of renal tubular epithelial cells

  • Authors:
    • Xin Wang
    • Jiaojiao Zhou
    • Jia Yang
    • Siwen Wang
    • Lichuan Yang
  • View Affiliations / Copyright

    Affiliations: Division of Nephrology, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, P.R. China, Division of Ultrasound, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, P.R. China
  • Article Number: 115
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    Published online on: September 18, 2020
       https://doi.org/10.3892/etm.2020.9243
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Abstract

The aim of the present study was to explore the role of toll‑like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88)/nuclear factor (NF)‑κB signaling in the contrast‑induced injury of renal tubular epithelial cells, and to investigate the potential mechanisms. HK‑2 cells cultured in vitro were randomly divided into six groups as follows: i) The blank group; ii) the iohexol group; iii) the NF‑κB RNAi group (NF‑κB siRNA + iohexol); iv) the TLR4 RNAi group (TLR4 siRNA + iohexol); v) the NF‑κB blocker group (PDTC + iohexol); and vi) the TLR4 blocker group (CLI‑095 + iohexol). The expression of the TLR4/MyD88/NF‑κB signaling pathway proteins was detected by reverse transcription‑quantitative (RT‑q)PCR and western blot analysis, and the cellular proliferation rate was determined using the Cell Counting Kit‑8 assay. The mRNA expression levels of the inflammatory cytokines tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β and IL‑6 were also detected using RT‑qPCR, and apoptosis was assessed by flow cytometry and western blotting to detect apoptosis‑associated proteins (caspase‑3, caspase‑9 and cleaved caspase‑9). Compared with the blank group, the apoptotic rates and the expression levels of TLR4, MyD88, NF‑κB, caspase‑3, cleaved caspase‑9, TNF‑α, IL‑1β and IL‑6 were upregulated in the iohexol group (P<0.001). However, when TLR4 or NF‑κB were blocked or silenced, these effects were reversed (P<0.001). Collectively, the results of the present study indicated that TLR4/MyD88/NF‑κB signaling is involved in the contrast‑induced injury of renal tubular epithelial cells by inducing inflammation and apoptosis.
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Copy and paste a formatted citation
Spandidos Publications style
Wang X, Zhou J, Yang J, Wang S and Yang L: Role of TLR4/MyD88/NF‑&kappa;B signaling in the contrast‑induced injury of renal tubular epithelial cells. Exp Ther Med 20: 115, 2020.
APA
Wang, X., Zhou, J., Yang, J., Wang, S., & Yang, L. (2020). Role of TLR4/MyD88/NF‑&kappa;B signaling in the contrast‑induced injury of renal tubular epithelial cells. Experimental and Therapeutic Medicine, 20, 115. https://doi.org/10.3892/etm.2020.9243
MLA
Wang, X., Zhou, J., Yang, J., Wang, S., Yang, L."Role of TLR4/MyD88/NF‑&kappa;B signaling in the contrast‑induced injury of renal tubular epithelial cells". Experimental and Therapeutic Medicine 20.5 (2020): 115.
Chicago
Wang, X., Zhou, J., Yang, J., Wang, S., Yang, L."Role of TLR4/MyD88/NF‑&kappa;B signaling in the contrast‑induced injury of renal tubular epithelial cells". Experimental and Therapeutic Medicine 20, no. 5 (2020): 115. https://doi.org/10.3892/etm.2020.9243
Copy and paste a formatted citation
x
Spandidos Publications style
Wang X, Zhou J, Yang J, Wang S and Yang L: Role of TLR4/MyD88/NF‑&kappa;B signaling in the contrast‑induced injury of renal tubular epithelial cells. Exp Ther Med 20: 115, 2020.
APA
Wang, X., Zhou, J., Yang, J., Wang, S., & Yang, L. (2020). Role of TLR4/MyD88/NF‑&kappa;B signaling in the contrast‑induced injury of renal tubular epithelial cells. Experimental and Therapeutic Medicine, 20, 115. https://doi.org/10.3892/etm.2020.9243
MLA
Wang, X., Zhou, J., Yang, J., Wang, S., Yang, L."Role of TLR4/MyD88/NF‑&kappa;B signaling in the contrast‑induced injury of renal tubular epithelial cells". Experimental and Therapeutic Medicine 20.5 (2020): 115.
Chicago
Wang, X., Zhou, J., Yang, J., Wang, S., Yang, L."Role of TLR4/MyD88/NF‑&kappa;B signaling in the contrast‑induced injury of renal tubular epithelial cells". Experimental and Therapeutic Medicine 20, no. 5 (2020): 115. https://doi.org/10.3892/etm.2020.9243
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