The effect of TLR4/MyD88 inhibition by salvianolic acid B on neuropathic pain following spinal cord injury in mice.

Spinal cord injury (SCI) is a common type of injury and about one half of the patients affected by SCI will suffer from neuropathic pain within a year after injury. However, the treatment effect of the neuropathic pain is far from satisfactory. Our study attempted to reveal whether SalB could relieve the neuropathic pain caused by SCI in mice by inhibiting the TLR4/MyD88 pathway. The mice were randomly divided into sham group, model group, high-dose treatment group and low-dose treatment group. The high- and low-dose groups received varying doses of SalB after modeling. The increase of pain sensitivity was evaluated by detecting paw withdrawal mechanical threshold and withdrawal thermal latency. mRNA and protein expression levels of TLR4 and myD88 were detected by using qRT-PCR and Western Blot, respectively. Compared with the model group, there was a significant reduction in paw withdrawal mechanical threshold and withdrawal thermal latency after SalB treatment; SalB reduced the release of TNF-α and SP by inhibiting the TLR4/MyD88 pathway in the mouse model of SCI. This not only resulted in lower pain, but also contributed to long-term relief of mechanical hyperalgesia.