Exosomes　derived　from　human　bone　marrow　mesenchymal　stem　cells　(BMSCs)　play　potential　protective　roles　in　spinal　cord　injury　(SCI).　However,　the　underlying　mechanisms　remain　not　fully　elucidated.　Herein,　we　isolated　exosomes　from　BMSCs,　and　exosome　morphology　and　marker　protein　levels　were　identified　by　transmission　electron　microscopy　(TEM)　and　Western　blot,　respectively.　PC12　cells　were　treated　with　lipopolysaccharide　(LPS)　to　construct　an　injury　model,　and　then　incubated　with　BMSCs-derived　exosomes.　We　found　that　exosome　incubation　increased　miR-9-5p　expression,　and　inhibited　apoptosis　and　the　levels　of　inflammation　cytokines　and　ER　stress　marker　proteins.　Moreover,　histone　deacetylase　5　(HDAC5)　was　identified　as　a　target　gene　of　miR-9-5p　by　dual-luciferase　reporter　gene　assay.　Exosomal　miR-9-5p　upregulated　fibroblast　growth　factor　2　(FGF2)　expression　by　inhibiting　HDAC5-mediated　FGF2　deacetylation.　Then,　it　was　observed　that　HDAC5　overexpression　or　FGF2　inhibition　reversed　the　inhibitory　effects　of　exosomal　miR-9-5p　on　apoptosis,　inflammation　and　ER　stress　in　PC12　cells.　Additionally,　an　SCI　rat　model　was　established　and　exosomes　were　injected　for　treatment.　Exosomal　miR-95p　treatment　alleviated　locomotor　ability,　histopathological　damage,　neuronal　apoptosis,　inflammation　and　ER　stress　in　SCI　rats.　In　conclusion,　our　findings　indicated　that　exosomal　miR-9-5p　derived　from　BMSCs　promoted　FGF2　expression　by　inhibiting　HDAC5-mediated　deacetylation,　thus　inhibiting　LPS-induced　apoptosis,　inflammation,　and　ER　stress　in　PC12　cells,　and　alleviating　SCI　in　rat　model.　Our　study　may　provide　a　therapeutic　direction　for　SCI.