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Previous studies have shown that elevated protein O-GlcNAcylation is an endogenous stress response that benefits cell survival and promotes organ functional recovery.And Thiamet-G (O-G1cNAcase inhibitor) upregulates protein O-GlcNAcylation levels, has been shown to improve motor deficits in models of neurodegenerative diseases without any obvious detrimental side-effects.The aim of this study is to investigate the effects of protein O-GlcNAcylation upregulation on the spinal cord injury (SCI) of rats.SCI+Thiamet-G group was injected with Thiamet-G (1Omg/kg/once/day;i.v.) for 3 days and the control group(SCI+SS) group with saline solution.Locomotor behavior was assessed using the Basso,Beattice, and Bresnahan (BBB) scale.Histopathological alterations were evaluated by morphometry and histochemistry.Potential inflammatory effects were assessed by microglia/ macrophages immunohistochemistry,and potential apoptosis effects were assessed by caspase-3 western blot.Thiamet-G treatment induced elevated protein O-GlcNAcylation, improved hindlimb motor functional recovery, mitigated the severity and reduced the lesion size promoted the structural recovery of the injured spinal cord, inhibited microglia/macrophages infiltration at the injury sites,and inhibited the caspase-3 mediated apoptosis pathway.So these findings indicates that Thiamet-G induced elevated protein O-GlcNAcylation ameliorated acute SCI, which could provide a potential novel therapeutic approach for SCI treatment.