Bone morphogenetic protein 7 upregulates the expression of nestin and glial fibrillary acidic protein in rats with cerebral ischemia-reperfusion injury

Bone morphogenetic protein 7 (BMP7) is a member of the transforming growth factor-β (TGF-β) superfamily and was initially identified as a protein that may induce bone and cartilage growth in the bone matrix. The present study was conducted in order to investigate the effect of BMP7 on the expression of nestin and glial fibrillary acidic protein (GFAP) in the brain tissue of rats after cerebral ischemia-reperfusion injury. A total of 40 adult healthy male Sprague-Dawley rats were used in this study, of which 10 randomly received a sham operation and the remaining 30 were subjected to a 2-h ischemia and 24-h reperfusion by ligation of the left external and internal carotid arteries. Twenty successfully modeled rats were equally randomized into the treatment and control groups. The rats in the treatment group were intervened with 250 μl BMP7 (0.1 mg/kg) via tail vein injection, whereas the rats in the control and sham operation groups were injected with an equal volume of sterile water for injection. Neurological deficits were evaluated by the Bederson's method at 24 h after ischemia-reperfusion and the brain infarct volume was assessed by 2,3,5-triphenyl tetrazolium chloride coloring. The neuronal apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nick end-labelling (TUNEL) staining and the expression of nestin and GFAP in the three groups was analyzed by immunohistochemistry. Bederson's score (t=4.66, P<0.01) and focus infarction (t=6.98, P<0.01) were lower in the BMP7 treatment group compared to those in the control group. In addition, the number of TUNEL-positive cells in the treatment group was lower compared to that in the control group (P<0.01). Compared to the control group, the expression of nestin and GFAP was enhanced in the BMP7 treatment group (P<0.01). Therefore, BMP7 may upregulate the expression of nestin and GFAP and promote neural regeneration to protect animals against ischemia-reperfusion injury.