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目的:观察促红细胞生成素(EP0)对新生缺氧缺血性脑损伤(HIBD)大鼠脑组织Bcl-2及Bax蛋白表达的影响,探讨EPO神经保护作用的分子机制。方法:42只7d龄新生Wistar大鼠随机分为假手术组、HIBD组、生理盐水对照组、EPO干预组,其中EPO干预组又分大、中、小剂量3组。建立HIBD模型后,立即一次性腹腔注射不同剂量(10000U/kg、5000U/kg、1000U/kg)的人基因重组促红细胞生成素(rhEPO),用免疫组织化学方法观察给药24h后脑组织Bcl-2及Bax蛋白表达的变化。结果:大鼠缺氧缺血后,脑组织Bcl-2及Bax蛋白表达均显著增高,Bcl-2/Bax显著降低,EPO干预后Bcl-2蛋白表达增加,Bcl-2/Bax显著增高,Bax蛋白表达显著降低,差异均有统计学意义。结论:EPO可以通过上调Bcl-2蛋白表达及下调Bax蛋白表达,改变Bcl-2/Bax比值,抑制细胞凋亡而起到神经保护作用,为临床治疗新生儿HIBD提供了更有意义的理论依据。
Objective: To observe the effect of erythropoietin (EPO) on the protein expression of Bcl-2 and Bax in brain tissue of neonatal hypoxic-ischemic brain damage (HIBD) rats and to explore the molecular mechanism of EPO neuroprotection. Methods: Forty-two newborn Wistar rats of 7 days old were randomly divided into sham operation group, HIBD group, saline control group and EPO intervention group. EPO intervention group was divided into three groups: large, medium and small doses. After establishment of HIBD model, human recombinant recombinant human erythropoietin (rhEPO) was injected intraperitoneally at different doses (10000U / kg, 5000U / kg and 1000U / kg) immediately after intraperitoneal injection of HIBD. The expression of Bcl- 2 and Bax protein expression changes. Results: After hypoxia / ischemia, the expression of Bcl-2 and Bax were significantly increased, Bcl-2 / Bax was significantly decreased, the expression of Bcl-2 protein, Bcl-2 / Protein expression was significantly reduced, the differences were statistically significant. CONCLUSION: EPO can provide neuroprotective effects by up-regulating the expression of Bcl-2 and down-regulating the expression of Bax, changing the ratio of Bcl-2 / Bax, and inhibiting the apoptosis of neonatal rats, providing a more meaningful theoretical basis for the clinical treatment of neonatal HIBD .