Related Experiment Video
Updated: Apr 26, 2026
A Neuronal Apoptosis Model induced by Spinal Cord Compression in Rat
Published on: June 29, 2021
Changes in autophagy proteins in a rat model of spinal cord injury
Qin Zhang1, Chen Huang, Bin Meng
1Department of Orthopaedics, Yuncheng Central Hospital, Yuncheng 044000, Shanxi Province, China.
Objective:
Autophagy is involved in several neurodegenerative diseases and recently its role in acute brain injury has won increasing interest. Spinal cord injuries (SCIs) often lead to permanent neurological deficit. Therefore, in this study, we examined the pro?les of autophagy-linked proteins (MAP-LC3) after SCI to investigate whether the expression of autophagy contributes to neurological deficit after SCI.
Methods:
Adult female Sprague-Dawley rats were used and randomly divided into control and SCI groups. All the rates received laminectomy at T8-T10 level. Those in the SCI group received additional exposure of the dorsal surface of the spinal cord, followed by a weight- drop injury. Thereafter we investigated the expression levels of MAP-LC3, beclin-1, Cathepsin D and the beclin-1-binding protein bcl-2 by western blot analysis at 12 h, 24 h, 3 d, 7 d, 21 d and 28 d. One-way ANOVA with Tukey post hoc test was used to compare data between groups.
Results:
We observed significant increase in the level of LC3 (LC3-II/LC3-I) at 3 d and 7 d after SCI when compared with the sham group. While the level of beclin-1 and ratio of beclin-1/bcl-2 was found to have increased from 12 h to 24 h after injury. Cathepsin D expression was also elevated at 7 d (P<0.01).
Conclusion:
Based on the above mentioned data, we proposed that autophagy plays a role in the manifestation of cell injury following SCI.
