Objectives: It is suggested that the injury-induced cell death of neurons within the spinal cord is related with endoplasmic reticulum (ER) stress. In this work, we explored that diabetes induce more severe spinal cord injury (SCI) and stronger ER stress in rats.
Methods: Forty-five Sprague-Dawley rats were divided into three groups at random (the sham operation control group, SCI group and diabetic SCI group). Streptozotocin was injected into the caudal vein (30 mg/kg) to induce diabetes; 4 weeks after diabetes model induction, using a weight-drop contusion model of SCI in SCI group and diabetic SCI group; then, rats were killed at 24 hours and 7 days, and the level of C/EBP homologous transcription factor protein (CHOP), a proapoptotic protein, and caspase 12 were determined by immunohistochemistry staining and real-time reverse transcription quantitative polymerase chain reaction analysis.
Results: We observe that both CHOP and caspase 12 were higher in diabetic SCI group than in the SCI group. Diabetes also caused severe locomotor dysfunction and slowly recovered as their Basso, Beattie and Bresnaha scores lowered. Pathological hematoxylin-eosin staining observation also showed progressive disruption of the dorsal white and few neurons regeneration in diabetic SCI rats.
Discussion: These results suggest that stronger ER stress in diabetic rats may be the reason for severe SCI observed.