Enolase inhibition reduces autophagy and promotes neurological function recovery after spinal cord injury

Abstract

Abstract Spinal cord injury (SCI) is a highly debilitating condition that impairs neuronal function and triggers a complex cascade of primary and secondary damage events. Autophagy can result in cell death, which is a phenomenon in eukaryotic cells and plays an important role in the development of SCI. Thus, this provides a practical and potential target for therapeutic intervention against SCI. Enolase inhibition (ENOblock) has been demonstrated to provide neuroprotection and functional recovery in a rat model of SCI. However, it remains unclear whether ENOblock can mediate neuronal autophagy after SCI. For rat model of SCI, All rats underwent laminectomy from T8 to T10. Sci rats were subjected to dorsal spinal cord exposure and SCI was injured using a modified Allen’s weight-drop apparatus. Locomotor function was assessed using the Basso, Beattie, and Bresnahan(BBB) rating scores. Thereafter we investigated the expression levels of autophagy-related proteins and Enolase by by western blot, immunofluorescence and quantitative polymerase chain reaction analysis. We found that the expression levels of autophagy-related proteins (LC3-Ⅱ and Beclin-1) and Enolase were significantly increased after acute SCI. In contrast, ENOblock could down-regulate the expression of these proteins and improve motor function after SCI. The difference between the SCI group and ENOblock group was most pronounced on the third and seventh day. Based on the above mentioned data, we speculate that ENOblock may play a role in inhibiting autophagy activity and promoting functional recovery after SCI in rats.