| Objectives Observe the global cerebral ischemia reperfusion in rats after different time points in the hippocampus Stromal-derived factor-1α(SDF-1α) and its receptor CXCR4 expression and apoptosis, and cobalt chloride(Cocl2) hypoxia preconditioning on its intervention effect, explore the cobalt chloride protective mechanisms of ischemic reperfusion.Methods Pulsinelli modified four-vessel occlusion prepared global cerebral ischemiareperfusion model, 180 male SD rats were randomly divided into sham group(sham group),the global cerebral ischemia reperfusion group(model group, GI group), hypoxia preconditioning group(HPC group). Hypoxia preconditioning group before making model by intraperitoneal injection of 2 h, 24 h, 48 h cobalt chloride solution(30 mg/kg). Between groups in ischemia reperfusion rats 6 h, 12 h, 24 h, 48 h, 72 h, 7 d 6 point observation, each point in time. Only 10 groups of rats in each observation point to death after separation of mouse brain tissue preparation of paraffin section, using HE staining were observed under brain tissue pathology change, in situ end labeling method(TUNEL) to observe the apoptosis of hippocampus neuron, immunohistochemical method to observe the hippocampus SDF-1α, the expression of CXCR4 positive neurons. Microscope count TUNEL staining positive on the number of apoptotic neurons in the brain and express SDF-1α and CXCR4 on the number of positive cells. The observed value to EXCEL database after finishing using SPSS17.0 statistical software package for data analysis. The analyzed result was expressed as mean±SD( x ±s).Group comparison using single factor analysis of variance, difference between two multiple comparison using SNK test.Results 1 Sham group in the hippocampus of rats accidentally see SDF-1α positive cells expression. Model group of hippocampus in cerebral ischemia reperfusion after each time all is obvious SDF-1α positive expression, and gradually increased with the extension of time expression, 7 d still have higher positive expression.Hypoxia precontrol group hippocampus SDF-1α positive cells were higher than in model group, the difference was statistically significant(P<0.05). Compared with sham group, model group and hypoxia precontrol in the hippocampus of rats accidentally see SDF-1α positive cells expression.Model group of hippocampus in cerebral ischemia reperfusion after each time all isobvious SDF-1α positive expression, and gradually increased with the extension of time expression, 7 d still have higher positive expression. Hypoxia preconditioning group at the same time points onditioning group each time point SDF-1α positive expression were higher, the difference was statistically significant(P<0.05). 2 The hippocampus of sham group have a small amount of CXCR4 positive cells expression. Model group each observation point the hippocampus after cerebral ischemia reperfusion CXCR4 positive expression were significantly increased, with the extension of reperfusion time appears to increase after the first reduce the change trend of 7 d reperfusion is still in the high level expression. Compared with model group, ischemia reperfusion after hypoxia preconditioning group each observation point positive cells expression in the hippocampus CXCR4 were higher than in model group, the difference was statistically significant(P<0.05). Compared with control group, model group and hypoxia preconditioning group CXCR4 positive expression were significantly increased at each time point, the difference was statistically significant(P<0.05). 3 Control the hippocampus have rarely TUNEL staining positive neurons express. Model group and hypoxia preconditioning group ischemia reperfusion after each time point of the hippocampus TUNEL staining positive neurons are clearly visible, with the extension of reperfusion time showed a trend of first rise after the fall of the apoptosis positive neurons, 7 d still have higher positive expression of apoptosis neurons. Each time point number of hypoxia preconditioning group TUNEL staining positive neurons in hippocampus compared with model group decreased significantly, the difference was statistically significant(P<0.05); Compared with sham group, model group and the hypoxia preconditioning group each time of TUNEL staining positive neurons express are increased, the difference was statistically significant(P<0.05).Conclusions 1 Whole brain ischemia reperfusion can cause nerve cell damage, cell apoptosis, cobalt chloride prediction of oxygen treatment can reduce rat whole cell apoptosis after cerebral ischemia reperfusion. 2 After cerebral ischemic reperfusion alpha SDF-1α and CXCR4 expression increased, cobalt chloride hypoxia preconditioning can obviously increase the expression of the biological axis. 3 Cobalt chloride hypoxia preconditioning can reduce the apoptosis of rats, reducing ischemia-reperfusion injury and is beneficial to the recovery of neural function, its mechanism may be related to increase in the rat hippocampus SDF-1α, CXCR4 expression. |
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