Schematic illustrating potential mechanisms of the anti-nociceptive effects induced by TIIAS on neuropathic pain. Peripheral nerve injury (like spinal nerve ligation) increases pro-inflammatory cytokines and induces glial activation in the spinal dorsal horn (A). The potential roles of TIIAS in spinal pain transmission are presented in (B). Peripheral nerve injury induces pro-inflammatory cytokines, causing the activation of spinal JNK pathway in astrocytes. The up-regulation of MCP-1 produced by astrocytes via JNK-mediated pathway after SNL may facilitate the glutamate-related synaptic transmission and enhance neuropathic pain. JNK activation could be the targeting sites of TIIAS. Down-regulation of JNK/MCP-1 may be involved in the anti-nociceptive effect of TIIAS on neuropathic pain. TIIAS, tanshinone IIA sulfonate; JNK, c-Jun N-terminal kinase; MCP-1, monocyte chemoattractant protein-1.