The activation of BDNF reduced inflammation in a spinal cord injury model by TrkB/p38 MAPK signaling.

Abstract

The aim of the present study was to investigate the pro-inflammation effects of brain-derived neurotrophic factor (BDNF) signaling in promoting inflammation following spinal cord injury (SCI) in rats. Reverse transcription-quantitative polymerase chain reaction was used to detect the expression of BDNF in SCI rats. The Basso, Beattie and Bresnahan (BBB) test was used and the water content of spinal cord were assessed to determine the effects of BDNF on SCI. BDNF expression was increased in SCI rats. In an in vitro model, overexpression of BDNF induced the protein expression of tyrosine kinase receptor B (TrkB) and suppressed that of phosphorylated (p-)p38, and reduced inflammation, as indicated by tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-18, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 levels. Conversely, the TrkB inhibitor ANA-12 suppressed the protein expression of TrkB and induced that of p-p38, and promoted inflammation (as indicated by TNF-α, IL-1β, IL-6, IL-18, iNOS and COX-2 levels) in an in vitro model of SCI by BDNF overexpression. In addition, the p38 inhibitor TA-0, suppressed p38 protein expression and reduced inflammation in an in vitro model of SCI by BDNF overexpression. Together, these data suggest that the pro-inflammation effects of BDNF/TrkB promoted inflammation in SCI through p38 signaling in rats.