| 新生大鼠缺氧缺血性脑损伤TLR4表达及与细胞凋亡的关系 |
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| 作者姓名： | 梁桂娟 王迎涛 刘艳红 唐成和 关海山 |
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| 作者单位： | 1.郑州人民医院新生儿科，河南 郑州 4500532.中国人民解放军153 医院检验中心，河南 郑州 4500423.新乡医学院第一附属医院新生儿科，河南 新乡 453003 |
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| 摘 要： | 目的通过检测TLR4在新生大鼠缺氧缺血性脑损伤（HIBD）中表达变化，并与凋亡情况对比，研究TLR4在新生儿缺氧缺血性脑损伤发病机制中的作用，为临床的进一步研究提供客观的实验依据。 方法选取80只7 d龄新生健康大鼠，随机分为实验组和对照组各40只。TUNEL法检测脑组织细胞凋亡状况，免疫组化SP法检测TLR4表达变化。 结果细胞凋亡缺氧缺血术后6 h阳性率上升，至24 h达到高峰，72 h和7 d表达下降。TlR4实验组于缺氧缺血6 h即出现阳性表达，12 h表达到峰值，24 h无明显变化，72 h和7 d表达下降。实验组与对照组在各时间点比较差异均有统计学意义（P<0.05）。TLR4与细胞凋亡呈正相关（r=0.452）。 结论新生大鼠缺氧缺血性脑损伤组织中TLR4高表达，可能促进细胞凋亡发生，在脑损害的形成过程中起到了重要的作用。
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| 关 键 词： | 新生大鼠 缺氧缺血 脑损伤 TLR4 凋亡 |
| 收稿时间： | 2016-02-01 |
The correlation between TLR4 expression and apoptosis of hypoxic ischemic brain damage in neonatal rats |
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| Authors: | Guijuan LIANG Yingtao WANG Yanhong LIU Chenghe TANG Haishan GUAN |
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| Affiliation: | 1.Department of Neonatology, The People's Hospital of Zhengzhou, Zhengzhou 450053, China2.Laboratory Center of the PLA No.153Hospital, Zhengzhou 450042, China3.Department of Neonatology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang 453003, China |
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| Abstract: | Objective To investigate the role of TLR4 in HIBD by observing the change of TLR4 expression and cell apoptosis after hypoxic-ischemic brain damage (HIBD)in a neonatal rat model, and provide an experimental foundation for the futher clinical research. Methods A total of 80 7day postnatal Sprague-Dawley rats were randomly divided into experimental group (n=40) and control group(n=40). The expression of TLR4 was tested by immunohistochemistry, the apoptotic hippocampus cellswere tested by TUNEL. Results The cell apoptosis and the expression of TLR4 increased at HI 6 h, and achieved the hightest increases at HI 12 h, and it continued to maintain the high level in HI 24 h, then decreased at HI 72 h、HI7 d group. There were significant differences of positive rate at different times compared with control group(P<0.05). There was a positive correlation between apoptosis and TLR4(r=0.452) in rats with hypoxic-ischemic brain damage. Conclusion TLR4 over expressed in HIBDcan promote cell apoptosis, and play an important role in the pathogenesis of HIBD. |
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