miRNA‑146a attenuates inflammation in an in vitro spinal cord injury model via inhibition of TLR4 signaling
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- Published online on: August 22, 2018 https://doi.org/10.3892/etm.2018.6645
- Pages: 3703-3709
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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.
