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Article

miRNA‑146a attenuates inflammation in an in vitro spinal cord injury model via inhibition of TLR4 signaling

  • Authors:
    • Ying Tan
    • Longtan Yu
    • Chunming Zhang
    • Kebing Chen
    • Junfan Lu
    • Lei Tan
  • View Affiliations / Copyright

    Affiliations: Department of Spine Surgery, Weifang Traditional Chinese Medicine Hospital, Weifang, Shandong 261041, P.R. China, School of Medicine, Shandong University, Jinan, Shandong 250012, P.R. China, Department of Spine Surgery, Third Affiliated Hospital of Southern Medical University, Guangzhou, Guangdong 510430, P.R. China
  • Pages: 3703-3709
    |
    Published online on: August 22, 2018
       https://doi.org/10.3892/etm.2018.6645
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Abstract

The present study evaluated the anti‑inflammatory effect of microRNA (miR)‑146a in a spinal cord injury (SCI) rat model and in vitro model, and explored possible underlying mechanisms of this effect. miR‑146a expression was analyzed using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β and IL‑6 content was measured using ELISA kits. Inducible nitric oxide synthase (iNOS), prostaglandin E2 (PGE2), Toll‑like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88) and phosphorylated (p)‑nuclear factor (NF)‑κB were measured using western blotting. In the SCI rat model, miR‑146a expression was downregulated. In the in vitro model, downregulation of miR‑146a increased inflammation, enhanced iNOS and PGE2 protein expression and induced TLR4, MyD88 and NF‑κB expression. Overexpression of miR‑146a reduced inflammation, iNOS and PGE2 protein expression, and suppressed TLR4, MyD88 and NF‑κB expression in the in vitro SCI model. The inhibition of TLR4 attenuated the proinflammatory effects of anti‑miR‑146a in the in vitro SCI model. The results indicate that miR‑146a reduces inflammation in an SCI model through the TLR4‑NF‑κB signaling pathway. The present study demonstrated that miR‑146a may be a promising therapeutic agent for SCI.
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Copy and paste a formatted citation
Spandidos Publications style
Tan Y, Yu L, Zhang C, Chen K, Lu J and Tan L: miRNA‑146a attenuates inflammation in an in vitro spinal cord injury model via inhibition of TLR4 signaling. Exp Ther Med 16: 3703-3709, 2018.
APA
Tan, Y., Yu, L., Zhang, C., Chen, K., Lu, J., & Tan, L. (2018). miRNA‑146a attenuates inflammation in an in vitro spinal cord injury model via inhibition of TLR4 signaling. Experimental and Therapeutic Medicine, 16, 3703-3709. https://doi.org/10.3892/etm.2018.6645
MLA
Tan, Y., Yu, L., Zhang, C., Chen, K., Lu, J., Tan, L."miRNA‑146a attenuates inflammation in an in vitro spinal cord injury model via inhibition of TLR4 signaling". Experimental and Therapeutic Medicine 16.4 (2018): 3703-3709.
Chicago
Tan, Y., Yu, L., Zhang, C., Chen, K., Lu, J., Tan, L."miRNA‑146a attenuates inflammation in an in vitro spinal cord injury model via inhibition of TLR4 signaling". Experimental and Therapeutic Medicine 16, no. 4 (2018): 3703-3709. https://doi.org/10.3892/etm.2018.6645
Copy and paste a formatted citation
x
Spandidos Publications style
Tan Y, Yu L, Zhang C, Chen K, Lu J and Tan L: miRNA‑146a attenuates inflammation in an in vitro spinal cord injury model via inhibition of TLR4 signaling. Exp Ther Med 16: 3703-3709, 2018.
APA
Tan, Y., Yu, L., Zhang, C., Chen, K., Lu, J., & Tan, L. (2018). miRNA‑146a attenuates inflammation in an in vitro spinal cord injury model via inhibition of TLR4 signaling. Experimental and Therapeutic Medicine, 16, 3703-3709. https://doi.org/10.3892/etm.2018.6645
MLA
Tan, Y., Yu, L., Zhang, C., Chen, K., Lu, J., Tan, L."miRNA‑146a attenuates inflammation in an in vitro spinal cord injury model via inhibition of TLR4 signaling". Experimental and Therapeutic Medicine 16.4 (2018): 3703-3709.
Chicago
Tan, Y., Yu, L., Zhang, C., Chen, K., Lu, J., Tan, L."miRNA‑146a attenuates inflammation in an in vitro spinal cord injury model via inhibition of TLR4 signaling". Experimental and Therapeutic Medicine 16, no. 4 (2018): 3703-3709. https://doi.org/10.3892/etm.2018.6645
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