Spinal　cord　injury　(SCI)　is　a　major　cause　of　paralysis,　disability　and　even　death　in　severe　cases.　Lithium　has　neuroprotective　effects　on　SCI,　while　the　underlying　mechanisms　remain　obscure.　In　the　present　study,　we　established　a　SCI　rat　model,　which　subsequently　received　lithium　treatment.　Results　displayed　that　lithium　treatment　improved　the　locomotor　function　recovery　and　reduced　apoptosis　by　increasing　anti-apoptotic　molecule　expression　and　decreasing　pro-apoptotic　factor　expression　in　SCI　rats.　Furthermore,　lithium　treatment　alleviated　the　inflammatory　response　by　inactivating　the　nuclear　factor-kappa　B　(NF-kappa　B)　pathway　and　inhibited　the　expression　of　lncRNA　brain-derived　neurotrophic　factor　antisense　(BDNF-AS)　in　SCI　rats.　Subsequent　researches　indicated　that　miR-9-5p　was　targeted　and　regulated　by　BDNF-AS.　Lithium　treatment　rescued　the　upregulation　of　BDNF-AS　expression　and　downregulation　of　miR-9-5p　expression　induced　by　H2O2　in　SH-SY5Y　cells.　BDNF-AS　overexpression　or　miR-9-5p　interference　attenuated　the　anti-apoptotic　and　anti-inflammatory　effects　of　lithium　chloride　in　SH-SY5Y　cells　that　was　damaged　by　H2O2　induction,　revealing　that　lithium　might　act　through　the　BDNF-AS/miR-9-5p　axis.　In　vivo　studies　showed　that　the　injection　of　BDNF-AS　adenovirus　vector　or　miR-9-5p　inhibitor　reversed　the　effects　of　lithium　on　the　histologic　morphology　of　spinal　cord,　motor　function,　inflammatory　reaction　and　apoptosis　in　SCI　rats,　which　was　consistent　with　the　results　of　in　vitro　studies.　In　conclusion,　our　data　demonstrated　that　lithium　reduced　SCI-induced　apoptosis　and　inflammation　in　rats　via　the　BDNF-AS/miR-9-5p　axis.