EXPRESS: Propofol alleviates spinal cord ischemia-reperfusion injury by preserving PI3K/AKT/GIT1 axis.

Spinal cord ischemia-reperfusion injury (SCIRI) is a major contributor for neurological damage and mortality associated with spinal cord dysfunction. This study aims to explore the possible mechanism of Propofol and GIT1 in regulating SCIRI in rat models. SCIRI rat models were established and injected with Propofol, OE-GIT1 or PI3K inhibitor (LY294002). The neurological function was assessed using Tarlov scoring system and H&E staining was applied to observe morphology changes in spinal cord tissues. Cell apoptosis, blood-spinal cord barriers (BSCB) permeability and inflammatory cytokines were determined by TUNEL staining, EB staining and ELISA, respectively. RT-qPCR and western blot were used to detect the expression levels of GIT1, eNOS, PI3K/AKT signal pathway and apoptosis-related proteins. SCIRI rats had decreased expressions of GIT1 and PI3K/AKT-related proteins, whose expressions can be elevated in response to Propofol treatment. LY294002 can also decrease GIT1 expression level in SCIRI rats. Propofol can attenuate neurological dysfunction induced by SCIRI, decrease spinal cord tissue injury and BSCB permeability in addition to suppressing cell apoptosis and inflammatory cytokines, whereas further treatment by LY294002 can partially reverse the protective effect of Propofol on SCIRI. Propofol can activate PI3K/AKT signal pathway to increase GIT1 expression level, thus attenuating SCIRI in rat models.