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Abstract
Objectives: Spinal cord injury (SCI) is associated with high morbidity and mortality worldwide, especially in patients with diabetes mellitus. Thrombospondin 1 (TSP-1) is a mutual activator and can cause neuron injury during hyperglycemia. We investigated the role of TSP-1 in a model of diabetic rats in the development of SCI.
Methods: Thirty Sprague–Dawley female rats were divided into three groups (SCI group, SCI + diabetes group and sham-operated group) at random. Ten rats were intraperitoneally injected with streptozocin (60 mg/kg) to induce diabetes; the remaining 20 rats received an injection of 0.9% saline as SCI group and the third group was sham-operated group. Four weeks later, ten rats in the SCI group and ten diabetic rats were subjected to SCI using an impactor, and the sham-operated group was also followed at the same time course without SCI. These animals were killed at 12 hours after SCI for immunochemistry and Western blot analysis of the injured section for the expression of TSP-1 protein. Morphological changes of spinal cord in three groups also were observed through hematoxylin–eosin staining. All data were analysed by t-test.
Results: The data of weight and blood sugar indicated no significant difference in all three groups before animal model induction. Four weeks after the induction of diabetes, the differences between the SCI and SCI + diabetes groups in weight and blood sugar were distinct. Immunochemistry and Western blot analysis showed increased TSP-1 expression in SCI group when compared with the sham-operated group rat but less than the SCI + diabetes group (p<0.01). The pathological alterations, such as central core lesion with a spare peripheral rim of tissue, and variable cyst formations and gliosis were very apparent in the damaged spinal cord area in the SCI group and especially in the SCI + diabetes group.
Discussion: Our work provides experimental evidence that the elevated expression of TSP-1 can be detected in the injured segment of the spinal cord at 12 hours after injury in diabetic rats. It may contribute to severe damage in diabetic rats after SCI.