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目的:观察促红细胞生成素(EPO)对短暂性全脑缺血再灌注后海马CA1区iNOS蛋白表达的影响,探讨其对缺血脑组织保护的可能机制。方法:应用四动脉血流阻断法制作大鼠短暂性全脑缺血再灌注模型;于再灌注开始时经腹腔注射EPO(3000U/kg);48h灌注取脑。苏木精—伊红染色和TUNEL法染色观察海马CA1区神经细胞坏死和凋亡。应用免疫组织化学方法检测iNOS蛋白的表达。结果:短暂性全脑缺血15min再灌注后48h,苏木精—伊红染色海马CA1区存活神经元细胞数正常组(211.28±7.95)个/视野,假手术组为(209.28±11.34)个/视野,EPO治疗组海马CA1区存活神经元细胞数为(170.28±8.12)个/视野,缺血组为(146.84±8.35)个/视野。EPO治疗组与缺血组比较差异有显著性意义(P<0.01)。TUNEL法凋亡细胞测定,正常组无阳性细胞,假手术组阳性细胞(152.48±18.52)个/视野,EPO治疗组有(1797.51±151.35)个/视野,缺血组有(2250.41±180.06)个/视野,两者比较差异有显著性意义(P<0.01)。iNOS蛋白的表达测定,正常组无阳性细胞,假手术组海马CA1区阳性细胞区灰度值为5.36±1.54,EPO治疗组为31.80±6.42,缺血组为49.46±8.96。EPO治疗组与缺血组比较,两者差异有显著性意义(P<0.01)。结论:EPO可减少大鼠短暂性全脑缺血再灌注后神经元的死亡和凋亡,抑制iNOS
Objective: To observe the effect of erythropoietin (EPO) on the expression of iNOS protein in hippocampal CA1 area after transient global cerebral ischemia-reperfusion in rats and to explore its possible mechanism of protection on ischemic brain tissue. Methods: The model of transient global cerebral ischemia-reperfusion was established by four-artery blockade. EPO (3000U / kg) was injected intraperitoneally at the beginning of reperfusion and the brain was infused at 48h. Hematoxylin-eosin staining and TUNEL staining were used to observe neuronal cell apoptosis and apoptosis in hippocampus CA1 area. Immunohistochemistry was used to detect the expression of iNOS protein. Results: After transient ischemic brain injury 15 min and 48 h after reperfusion, the number of surviving neurons in the hippocampal CA1 region was (211.28 ± 7.95) / visual field, and the sham group was (209.28 ± 11.34) / Field of vision, EPO treatment group hippocampal CA1 area survival neuronal cell number (170.28 ± 8.12) / field, ischemic group (146.84 ± 8.35) / field. There was significant difference between EPO treatment group and ischemia group (P <0.01). TUNEL assay showed that there were no positive cells in the normal group and 152.48 ± 18.52 cells in the sham operation group (1797.51 ± 151.35) / field in the EPO group and 2250.41 ± 180.06 in the ischemic group / Visual field, the difference between the two was significant (P <0.01). The expression of iNOS protein in normal group was lower than that in normal group. The gray value of CA1 positive cell in hippocampus in sham operation group was 5.36 ± 1.54, that in EPO group was 31.80 ± 6.42, and in ischemic group was 49.46 ± 8.96. EPO treatment group compared with ischemic group, the difference was significant (P <0.01). Conclusion: EPO can reduce neuronal death and apoptosis after transient global cerebral ischemia-reperfusion in rats, and inhibit iNOS