Aucubin promoted neuron functional recovery by suppressing inflammation and neuronal apoptosis in a spinal cord injury model

•Aucubin is beneficial to the recovery of motor function after spinal cord injury in rats.•Aucubin promotes the polarization ratio of M2/M1 in microglia to reduce the release neuroinflammation and inhibits neuronal apoptosis in vivo and in vitro.•Aucubin regulates microglial polarization by activating the TLR4/NF-κB pathway and is validated by turn-over experiments.•Aucubin improve neuronal apoptosis by reverse mitochondrial dysfunction. Spinal cord injury (SCI) can cause severe motor impairment. Post-SCI treatment has focused primarily on secondary injury, with neuroinflammation and neuronal apoptosis as the primary therapeutic targets. Aucubin (Au), a Chinese herbal medicine, exerts anti-inflammatory and neuroprotective effects. The therapeutic effects of Aucubin in SCI have not been reported. In this study, we carried out an in vivo SCI model and a series of in vitro experiments to explore the therapeutic effect of Aucubin. Western Blotting and immunofluorescence were used to study the effect of Aucubin on microglial polarization and neuronal apoptosis and its underlying mechanism. We found that Aucubin can promote axonal regeneration by reducing neuroinflammation and neuronal apoptosis, which is beneficial to motor recovery after spinal cord injury in rats. Our further in vitro experiments showed that Aucubin can activate the toll-like receptor 4 (TLR4)/myeloid differentiation protein-88 (MyD88)/IκBα/nuclear factor kappa B (NF-κB) signaling pathway to reduce neuroinflammation and reverse mitochondrial dysfunction to reduce neuronal apoptosis. In summary, these results suggest that Aucubin may ameliorate secondary injury after SCI by reducing neuroinflammation and neuronal apoptosis. Therefore, Au may be a promising post-SCI therapeutic drug.