摘要
目的:探讨慢性低O_2高CO_2对大鼠海马神经细胞TLR4和NFκB的影响及作用。方法:采用慢性低O_2高CO_2肺动脉高压大鼠模型,30只大鼠随机分为正常对照组(NC)、低O_2高CO_22周组(2HH组)和低O_2高CO_24周组(4HH组),免疫组织化学法检测海马CA1/3区细胞TLR4和NFκB的表达,TUNEL法检测海马细胞凋亡。结果:模型组大鼠海马CA1/3区TLR4蛋白的表达随着时间延长而显著,2HH组(CA1:0.1275±0.0242,CA3:0.1156±0.0376),4HH组(CA1:0.1522±0.0187,CA3:0.1427±0.0453),与NC组比较有显著性差异(P<0.05,P<0.01)。NC组大鼠海马CA1/3区可见NFκB/p65少量表达于胞浆,而模型组可见NFκB/p65在细胞核内不同程度表达,2HH组(CA1:0.1326±0.0324,CA3:0.1301±0.0112),4HH组(CA1:0.1612±0.0428,CA3:0.1578±0.0365),与NC组比较分别有显著性差异(P<0.05,P<0.01)。模型组大鼠海马CA1/3区细胞凋亡明显增多,与NC组比较分别有显著性差异(P<0.01),以4HH组为著。结论:TLR4和NFκB激活可能在慢性低O_2高CO_2大鼠海马神经细胞凋亡中有重要作用。
Aim： To study the expression and effect of TLR4 and NFκB protein in hippoeampus neuron in mrs exposed to chronic hypoxie hypercapnia. Methods： The disorder of learning-memory in pulmonary hypertension rat model was reproduced by chronic hypoxie hypereapnia. Thirty rats were randomly divided into three groups： normal control group, hypoxic hypercapnia 2-week and 4-week group. The number of apoptosis neurons in hippoeampus CA1/3 was counted by TUNEL method. Activity of TLR4 and NFκB in hippocampus CA1/3 was deeteeted by using SP immunoeytoehemieal technique. Results： The expression of TLR4 protein in hippoeampus CA1/3 in group 2HH（ CAI：0. 1275 ± 0. 0242, CA3：0.1156 ± 0. 0376） and 4HH（ CA1：0. 1522 ±0. 0187, CA3： 0. 1427 ± 0.0453） were significantly higher than those in the NC group（ P 〈 0.05, P 〈 0.01 ）. The positive expression of NFκB were showed in cell nueleus in group 2HH（ CA1 ： 0. 1326 ± 0. 0324, CA3 ： 0.1301 ± 0.0112） and group 4HH （CA 1： 0. 1612 ± 0. 0428, CA3： 0. 1578 ± 0. 0365）, and significantly higher than those in the NC group（ P 〈 0.05 P 〈 0.01 ）. The apoptosis of neural cells in hippoeampus CA1/3 gradually increased with the time of exposure, and reached peak at 4 weeks （P〈 0.01 vs NC group）. Conclusion： The activation of TLR4 and NFκB may play an important role in the apoptosis of hippocampns neural cells in rat exposed to chronic hypoxic hypercapnia.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2009年第1期27-30,共4页
Chinese Journal of Applied Physiology
基金
浙江省自然科学基金资助项目(Y205233)
温州市科技厅课题资助项目(Y2005A152)
