Autophagy is degradation of intracellular proteins and organelles to maintain cytoplasmic homeostasis, and it is also involved in various pathophysiological processes in many diseases. We previously investigated alternation of autophagic activity in damaged neural tissue after SCI. It was also examined whether administration of rapamycin to promote autophagy can induce neuroprotective effect in SCI. Our results of these studies demonstrated that molecular markers of autophagy such as Beclin 1 and LC3 were significantly upregulated in the injured spinal cord. The increased activity of autophagy was observed in neurons, astrocytes, and oligodendrocytes at the lesion site. Electron microscopy showed an increased formation of autophagic vacuoles in the damaged neural cells. In addition, the rapamycin administration in acute phase of SCI promoted autophagy in the injured spinal cord and reduced neural tissue damage and locomotor impairment. These findings indicated that autophagic activity is increased in damaged neural tissue after SCI. Furthermore the promotion of autophagy by rapamycin treatment can provide neuroprotective effect to improve locomotor function following SCI. Here, we summarize our previous studies and review the evidence in related articles regarding the role of autophagy in SCI.
ASJC Scopus subject areas