Sparstolonin B attenuates spinal cord injury‑induced inflammation in rats by modulating TLR4‑trafficking.

The present study used a spinal cord injury (SCI) model to evaluate whether sparstolonin B was able to prevent SCI, and to investigate the underlying signaling mechanism. Sparstolonin B attenuated the SCI‑induced Batto, Beattie and Bresnahan score and water content in rats. Sparstolonin B attenuated the mRNA expression of proinflammatory cytokines interleukin (IL)‑18, IL‑6, IL‑1β, and IL‑23, decreased the levels of tumor necrosis factor‑α and interferon‑γ, and decreased caspase‑3 activity and apoptosis regulator Bax protein expression in SCI rats. Similarly, sparstolonin B inhibited monocyte chemoattractant protein‑1 mRNA levels, and Toll‑like receptor (TLR) 4, myeloid differentiation primary response protein MyD88 (MyD88) and nuclear factor (NF)‑κB protein levels in SCI rats. The present results suggested that sparstolonin B may attenuate SCI‑induced inflammation and apoptosis in rats by modulating the TLR4/MyD88/NF‑κB signaling pathway.