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目的探讨促红细胞生成素(EPO)对缺氧缺血性脑损伤(HIBD)新生大鼠缺血侧脑组织存活素表达的影响及神经保护机制。方法健康7日龄SD新生大鼠72只,随机分为假手术组(n=24)、对照组(n=24)及EPO治疗组(n=24)。采用结扎左侧颈总动脉并吸入80mL.L-1氧气2h制作新生大鼠HIBD动物模型,造模后1d、3d、7d和14d取其脑组织标本,应用免疫组织化学法及脱氧核糖核苷酸末端转移酶介导的原位末端标记法分别对存活素的表达和细胞凋亡指数(AI)进行检测。结果与假手术组相比,对照组1d、3d、7d和14d缺血侧脑皮质存活素表达的吸光度值[(1.43±0.68)vs(0.13±0.03);(3.68±1.04)vs(1.69±0.19);(4.29±1.50)vs(0.36±0.05);(3.70±1.16)vs(0.98±0.26),Pa<0.01]及细胞AI值[(14.2±2.7)%vs(8.4±1.6)%;(16.5±3.5)%vs(1.4±1.1)%;(18.8±4.7)%vs(1.6±0.8)%;(8.2±3.1)%vs(2.2±1.7)%,Pa<0.01]均明显升高;与对照组相比,EPO治疗组1d、3d的存活素表达明显升高[(3.38±1.30)vs(1.43±0.68);(7.52±1.94)vs(3.68±1.04),Pa<0.05],细胞AI值1d、3d、7d明显降低[(9.8±2.1)%vs(14.2±2.7)%;(9.6±2.9)%vs(16.5±3.5)%;(10.6±2.8)%vs(18.8±4.7)%,Pa<0.05]。结论 EPO可通过促进抗凋亡因子存活素的表达而减少HIBD后的细胞凋亡,发挥其神经保护作用。
Objective To investigate the effect of erythropoietin (EPO) on the expression of survivin in ischemic brain tissue of neonatal rats with hypoxic-ischemic brain damage (HIBD) and its neuroprotective mechanism. Methods Totally 72 SD neonatal 7-day-old SD rats were randomly divided into sham operation group (n = 24), control group (n = 24) and EPO treatment group (n = 24). The model of HIBD in neonatal rats was made by ligating the common carotid artery of the left side and inhaling 80mL.L-1 oxygen for 2h. The brain tissue samples were taken at 1d, 3d, 7d and 14d after the model was established. Immunohistochemistry and deoxyribonucleoside The expression of Survivin and the apoptosis index (AI) were detected by acid end-transferase mediated in situ end-labeling. Results Compared with the sham-operation group, the absorbance values of ischemic cortex survivin at 1d, 3d, 7d and 14d in the control group [(1.43 ± 0.68) vs (0.13 ± 0.03) vs (3.68 ± 1.04) vs (1.69 ± (4.29 ± 1.50) vs (0.36 ± 0.05); (3.70 ± 1.16) vs (0.98 ± 0.26), Pa <0.01] and cell AI [(14.2 ± 2.7)% vs (8.4 ± 1.6)%, respectively; (16.5 ± 3.5)% vs (1.4 ± 1.1)%; (18.8 ± 4.7)% vs (1.6 ± 0.8)%; (8.2 ± 3.1)% vs (2.2 ± 1.7)%, Pa <0.01] ; Compared with the control group, the survivin expression of EPO treatment group was significantly increased on the 1st and 3rd day [(3.38 ± 1.30) vs (1.43 ± 0.68) vs (7.52 ± 1.94) vs (3.68 ± 1.04), P <0.05] The cell AI decreased significantly at 1d, 3d, 7d [(9.8 ± 2.1)% vs (14.2 ± 2.7)%; (9.6 ± 2.9)% vs (16.5 ± 3.5)%; (10.6 ± 2.8)% vs (18.8 ± 4.7 )%, Pa <0.05]. Conclusion EPO can reduce apoptosis after HIBD by promoting the expression of anti-apoptotic factor survivin and exert its neuroprotective effect.