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-1, and IL-23, decreased the levels of tumor necrosis factor- and interferon-, 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)-B 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-B signaling pathway.