新生大鼠缺氧缺血性脑损伤TLR4表达及与细胞凋亡的关系
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7d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6h阳性率上升,至24 h达到高峰,72 h和7d表达下降。T1R4实验组于缺氧缺血6h即出现阳性表达,12h表达到峰值,24 h无明显变化,72 h和7d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(X0.452 )。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。
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 immunohistochemistty the apoptotic hippocampus cells were 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 HIBD can promote cell apoptosis, and play an important role in the pathogenesis of HIBD.
梁桂娟(1);王迎涛(2);刘艳红(1);唐成和(3);关海山(1)
基础医学神经病学、精神病学
新生大鼠缺氧缺血脑损伤LR4凋亡
梁桂娟(1);王迎涛(2);刘艳红(1);唐成和(3);关海山(1).新生大鼠缺氧缺血性脑损伤TLR4表达及与细胞凋亡的关系[EB/OL].(2017-12-07)[2025-08-21].https://chinaxiv.org/abs/201712.00573.点此复制
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