P 209 - C-terminal domain of tetanus toxin changes the apoptosis- and autophagy-related protein levels following spinal cord injury in rat brain

Abstract

Traumatic spinal cord injury (SCI) can lead to post-traumatic inflammation, oxidative stress, motor neuron apoptosis, necrosis and autophagy of tissue. To promote and enhance recovery after SCI, recent development of devices and therapeutic interventions are needed. The aim of the present study was to investigate the possible role of C-terminal domain of tetanus toxin (Hc-TeTx) on cell death mechanisms including apoptosis and autophagy following SCI. Thirty five adult rats were divided into five groups (n=7 each) as follows: control, sham, trauma (SCI), SCI+Hc-TeTx and SCI+methylprednisolone groups. The functional neurological deficits due to the SCI were assessed by behavioral analysis using the BBB open-field locomotor test. The alterations in pro-/anti-apoptotic and autophagy related-protein levels were measured by western blotting technique. In our study, Hc-TeTx promotes locomotor recovery and motor neuron survival of SCI rats. Hc-TeTx decreased expression of bax, bad, bak, cleaved caspase-3, Ask1 and autophagy-related proteins including Atg5 and LC3II in brain. Our study provides an evidence that cell death mechanisms play critical roles in SCI and non-toxic peptides may exert protective effect and decrease cell death following SCI.