Intrathecal siRNA against Ski-interacting protein attenuates nociception in a rat model of neuropathic pain

Neuropathic pain is characterized by hyperalgesia, allodynia and spontaneous pain. Previous studies have shown that Ski-interacting protein (SKIP) played an important role in neuronal survival and neuroprotection. However, its expression and function in neuropathic pain remains unknown. We found that the level of SKIP was increased in the spinal cord in a time dependent manner after chronic constriction injury (CCI). Intrathecal injection of siRNA-SKIP inhibited the expression of SKIP and pro-inflammatory factors (TNF-α, IL-1β and IL-6), and alleviated mechanical allodynia and thermal hyperalgesia in CCI model of rats. In addition, siRNA-SKIP markedly suppressed the upregulation of β-catenin induced by the neuropathic pain. Taken together, our findings suggest that siRNA against SKIP can alleviate the chronic neuropathic pain through Wnt/β-catenin signaling pathway. Targeting SKIP may be a potential treatment for chronic neuropathic pain.