Arctigenin Suppresses Inflammation And Plays A Neuroprotective Effect In Mice With Spinal Cord Injury

Inflammation plays a key role in secondary injury after spinal cord injury (SCI) leading to spinal cord demyelination and neuronal death. Previous studies have shown that arctigenin markedly inhibits the phosphorylation of MAPKs and the activation of NF-kappa B, and reduced the expression of IL-1, IL-6, and TNF-alpha, resulting in anti-inflammatory effects. However, it remains unclear whether arctigenin can be used to treat SCI. In the present study, SCI mice were treated with different concentrations of arctigenin, and their motor functional recovery, neuronal density, microglial activation, and inflammatory cytokine levels were investigated. We found that arctigenin improved the basso mouse scale score, regularity index, and MaxContact area, and enhanced the amplitude of motor evoked potentials, promoted functional recovery in a dose and time-dependent manner in the SCI mice. In addition, arctigenin protected the neurons in a dose-dependent manner. Furthermore, arctigenin inhibited microglial activation, down-regulated the expression of TNF-alpha, IFN-gamma, IL-17, MCP-1, IL-6, and G-CSF, and the effect became more obvious as the concentration of arctigenin increased. In conclusion, arctigenin plays a neuroprotective role by inhibiting the activation of microglia, and reducing the expression of inflammation in the early stage of SCI in mice.