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目的建立3日龄SD大鼠缺氧缺血(HI)脑损伤模型,探讨HI对脑皮质细胞损伤及神经功能的影响。方法 3日龄新生大鼠随机分为HI组(n=35)与正常对照组(n=18)。HI组予右侧颈总动脉结扎,然后暴露于60mL.L-1氧气、37℃环境中,缺氧2.5h即建立模型。HI后24h采用免疫组织化学染色法检测各组皮质肿瘤坏死因子-受体1(TNF-R1)、Caspase-3的表达,HI后7d采用HE染色评估其神经病理学变化。其余大鼠HI后测试负趋反射时间与睁眼时间以评估神经功能发育情况。应用SPSS12.0软件进行统计学分析。结果免疫组织化学显示HI后24h,HI组损伤侧皮质可见大量TNF-R1、Caspase-3阳性细胞,显著高于对照侧与正常对照组(P<0.01);HE染色可见HI组HI后7d神经细胞固缩、变性、坏死;神经行为学评估可见HI组大鼠负趋反射时间延迟;HI组大鼠损伤侧睁眼时间[(18.1±1.0)d]延迟,明显晚于对照侧[(13.5±0.2)d]及正常对照组[(12.8±0.2)d](P<0.01)。结论 TNF-R1外源性凋亡信号通路参与未成熟脑皮质损伤。HI引起的神经细胞凋亡将导致以后的神经功能障碍。
Objective To establish a hypoxic-ischemic (HI) brain injury model of 3-day-old SD rats and investigate the effect of HI on the injury and neurological function of cerebral cortical cells. Methods 3-day-old neonatal rats were randomly divided into HI group (n = 35) and normal control group (n = 18). In the HI group, the right common carotid artery was ligated and then exposed to 60mL.L-1 oxygen. The model was established at 37 ℃ in hypoxia for 2.5h. The expression of tumor necrosis factor-receptor 1 (TNF-R1) and caspase-3 in cortex were detected by immunohistochemical staining 24h after HI. The neuropathological changes were assessed by HE staining 7 days after HI. The rest of rats were tested for negative reflex time and eye opening time to assess neurological development. Application SPSS12.0 software for statistical analysis. Results Immunohistochemistry showed that a large number of TNF-R1 and Caspase-3 positive cells were found in HI group at 24h after HI, which were significantly higher than those in control group and normal control group (P <0.01) Neurological behavior assessment showed delayed negative reflex in HI rats; the delayed eye opening time in injured group was (18.1 ± 1.0) d in HI group, which was significantly later than that in control group [(13.5 ± 0.2) d] and normal control group [(12.8 ± 0.2) d] (P <0.01). Conclusion TNF-R1 extrinsic apoptotic signaling pathway is involved in immature cerebral cortex injury. Neuronal apoptosis caused by HI will lead to subsequent neurological dysfunction.