摘要
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 brain hypoxic-ischemic （HI） model using postnatal day 3（P3） SD rats and evaluate the apoptotic neuronal cells in cerebral cortex and neurofunctional development.Methods The P3 rats were randomly divided into HI group （n=35） and control group（n=18）.HI was induced in P3 rats with right carotid artery ligation followed by 2.5 h hypoxia in 60 mL·L^-1 oxygen at 37 ℃.The injury of neural cells in the cerebral cortex was evaluated by tumor necrosis factor receptor-1（TNF-R1）,Caspase-3 immunostaining and Hematoxylin-Eosin （HE） staining in 24 h and 7 d after HI,respectively.Furthermore,the neurofunctional development was evaluated by negative geotaxis reflex and eye opening time.The data were analyzed by SPSS 12.0 software.Results Caspase-3 and TNF-R1 positive cells were abundant in the ipsilateral cortex at 24 h after HI,compared with contralateral part and control group（P〈0.01）.The neuronal degeneration and loss were also observed by HE staining on 7 d after HI.Furthermore,HI group showed the retarded performance in geotaxis reflex,the time of eye opening was longer in ipsilateral eye than that of contralateral part and control group [（18.1±1.0） d vs （13.5±0.2） d and （12.8±0.2） d,P〈0.01].Conclusions The TNF-R1 related extrinsic signalling pathway is involved in cerebral cortex injury of neonatal HI rats,which may lead to the subsequent neurofunctional deficits.
出处
《实用儿科临床杂志》
CAS
CSCD
北大核心
2010年第15期1174-1176,共3页
Journal of Applied Clinical Pediatrics
关键词
缺氧缺血
皮质
神经发育
大鼠
新生
hypoxia-ischemia
cerebral cortex
neurofunctional development
neonatal rat
