端粒重复序列结合因子2在新生鼠缺氧缺血脑损伤中的表达及作用被引量：2

The role of TRF2 on the neonatal rats with HIBD

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摘要目的研究端粒重复序列结合因子2(Telomere repeat binding factor 2,TRF2)在新生大鼠缺氧缺血脑损伤(Hypoxic ischemic brain damage,HIBD)中的表达情况,探讨TRF2在调控神经元凋亡中的作用。方法构建新生大鼠HIBD模型,于建模后2h、12h、24h和72h收集脑组织标本,采用免疫组化检测四个时间点HIBD新生大鼠脑组织中TRF2、p-Chk2、Chk2和Bax的表达,然后利用Western blot技术检测HIBD新生大鼠右侧脑组织中TRF2和Bax蛋白的表达。结果在新生大鼠缺氧缺血2h后,TRF2、p-Chk2和Bax的表达开始升高,并于24h时达到表达高峰,而Chk2的表达没有明显变化。Western blot证实缺氧缺血大鼠脑组织中TRF2和Bax蛋白在缺氧缺血后2h开始升高,于24h达到表达高峰。结论新生大鼠HIBD使TRF2表达显著升高,可能通过激活Chk2和Bax蛋白诱导神经元凋亡。 Objective To study the expression of the telomere repeat binding factor 2 （TRF2） in the neonatal rats with hypoxic ischemic brain damage （HIBD）, and explore the role of TRF2 in neuronal apoptosis. Methods HIBD model in neonatal rats was established, ipsilateral brains were collected 2h, 12h, 24h, and 72h after hypoxic-ischemic （HI） insult. The expression of TRF2, p-Chk2, Chk2, and Bax was detected through immunohistochemistry （IHC） and western blotting. Results The expression of TRF2, p-Chk2, and Bax was up-regulated from 2h to 72h, and peaked at 24h after HI. However, there was no significant change in the expression of Chk2. Conclusion HI induces significant up-regulation of TRF2 in neonatal rats. TRF2 might regulate neuronal apoptosis through the activation of Chk2 and Bax.

作者李世平邓嫒嫒屈艺赵凤艳母得志

机构地区四川大学华西第二医院儿科.出生缺陷与相关妇儿疾病教育部重点实验室

出处《西部医学》 2017年第1期13-16,共4页 Medical Journal of West China

基金国家自然科学基金(81330016 81270724) 国家临床重点专科建设项目(1311200003303) 四川省科技厅公益民生项目(2014SZ0149)

关键词 HIBD TRF2 CHK2 Bax 神经元凋亡 HIBD TRF2 Chk2 Bax Neuronal apoptosis

分类号 R722.19 [医药卫生—儿科]

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