Abstract
Spinal cord injury (SCI) is one major cause of death and results in long-term disability even in the most productive periods of human lives with few efficacious drugs. Autophagy is a potential therapeutic target for SCI. In the present study, we examined the role of lithium in functional recovery in the rat model of SCI and explored the related mechanism. Locomotion tests were employed to assess the functional recovery after SCI, Western blotting and RT-PCT to determine the level of p-ERK and LC3-II as well as p62, immunofluorescence imaging to localize LC3 and p62. Here, we found that both the expression of LC3-II and p62 were increased after SCI. However, lithium chloride enhanced the level of LC3-II while abrogated the abundance of p62. Furthermore, lithium treatment facilitated ERK activation in vivo, and inhibition of MEK/ERK signaling pathway suppressed lithium-evoked autophagy flux. Taken together, our results illustrated that lithium facilitated functional recovery by enhancing autophagy flux.