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
he role of TRF2 in the neonatal rats with HIBD
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，于建模后不同时间点收集脑组织标本，采用免疫组化检测各个时间点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是达到表达高峰，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 constructed, ipsilateral brains were collected on different time points after hypoxic-ischemic (HI) insult. The expression of TRF2, p-Chk2, Chk2, and Bax was detected by 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.
母得志、邓媛媛、赵凤艳、李世平、屈艺
基础医学神经病学、精神病学
HIBDRF2hk2Bax神经元凋亡
HIBDTRF2Chk2BaxNeuronal apoptosis
母得志,邓媛媛,赵凤艳,李世平,屈艺.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[EB/OL].(2015-12-07)[2025-08-18].http://www.paper.edu.cn/releasepaper/content/201512-345.点此复制
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