Effect of bone morphogenetic protein-7 on expression of Caspase-3 in rats with cerebral ischemic reperfusion injury

Objective: To explore the effect and the mechanism of bone morphogenetic protein-7 (BMP-7) on neuronal apoptosis in the rat brain after cerebral ischemic reperfusion injury. Methods: Ten rats from 40 adult healthy male Sprague-Dawley rats received sham-operation, and the other 30 rats were subjected to middle cerebral artery occlusion (MCAO) for 2 hours, of which the 20 successfully modeled rats were equally randomized into the control group and the treatment group, 10 rats each group. The rats in the treatment group were intervened with 250μl of BMP-7 (0.1 mg/kg) via caudal vein injection, while the rats in the control group and the sham-operative group were intervened with equal volume of normal saline. Animals were sacrificed at the 24th hour after reperfusion. Neurological deficits were evaluated by Bederson method, and the infarction volume of brain was investigated by 2,3,5-triphenyl tetrazolium chloride coloring. Pathological changes in the lesion site were investigated by HE coloring. The neuronal apoptosis was detected by TUNEL staining and the expression of Caspase-3 with the immunohistochemistry method. Results: In the treatment group, the Bederson score (1.7 ± 0.5, t = 4.66, P < 0.01) and focus infarction [(7.6 ± 1.4) %, t = 6.98, P < 0.01] were lower than those in the control group [2.7 ± 0.5, (22.3 ± 4.5) %]. Damage of the ischemia brain was significantly lessened in the BMP-7 treatment group. The number of TUNEL positive cells in the cortex (3.6 ± 0.6), striatum (7.4 ± 1.1) and hippocampus (5.0 ± 0.7) of the treatment group were lower than those in the control group (13.4 ± 1.1, 17.8 ± 1.5, 15.4 ± 1.1, P < 0.01). The number of Caspase-3 positive cells in the cortex (7.6 ± 0.9), striatum (5.8 ± 0.8) and hippocampus (10.6 ± 1.1) of the treatment group were lower than those in the control group (15.4 ± 0.6, 14.0 ± 1.2, 17.2 ± 0.8, P < 0.01). Conclusion: BMP-7 may down-regulate the expression of Caspase-3, and inhibit the neuronal apoptosis in order to protect animals against ischemia injury.