缺氧预处理新生大鼠缺氧缺血脑组织中Limk1蛋白表达  

Expression of Limkl in brain tissues of hypoxia-preconditioned hypoxicischemic neonatal rat models

作　　者：曾志涌 郑平 

机构地区：[1]深圳市龙岗区第二人民医院儿科,广东深圳518122

出　　处：《广州医学院学报》2011年第2期10-12,16,共4页Academic Journal of Guangzhou Medical College

基　　金：深圳市科技计划项目资助(201002159)

摘　　要：目的:观察Limk1蛋白在缺氧预处理后不同时间段新生大鼠缺氧缺血和对照组脑组织中的表达差异。方法:采用7日龄SD大鼠54只,随机分为于单纯缺血缺氧组18只,假手术对照组18只,缺氧预处理组18只。各组再分为处理后0 h、1d、7d组,每组各6只。用免疫组化法检测观察Limk1在不同组脑组织各部位的表达差异。结果:Limk1蛋白阳性神经元在各组的吸光度:单纯缺血缺氧组0 h(21.658±3.990)、1 d(30.369±5.156)、7 d(41.546±5.677);缺氧预处理组0 h(30.261±4.266)、1d(43.129±5.785)、7 d(56.309±7.198);假手术组0h(14.113±2.983)、1 d(16,098±3.116)、7d(15.983±3.009)。在单纯缺血缺氧组及缺氧预处理组脑组织的表达比假手术组增多(P<0.01)。在同一时间段上,缺氧预处理组比单纯缺血缺氧组Limk1的表达明显增多(P<0.01)。同样在缺血缺氧后,无论是单纯缺血缺氧组还是缺氧处理组,Limk1的表达随着0 h、1、7 d的推移表达渐增多(P<0.05)。结论:缺氧预处理能够增加新生大鼠缺血缺氧性脑组织中Limk1的表达,其提示缺氧预处理后的新生大鼠缺血缺氧的脑组织可能存在更强的神经重塑作用。Objective：To study the differential expression of LIM-kinase 1 （ Limk1 ） at different time spots after hypoxia preconditioning in brain tissues of hypoxic-ischemic neonatal rat models and controls. Methods： Seven-day-old SD rats were randomized into pure hypoxia-ischemia group, sham operation group, and hypoxia- preconditioned group（n = 18 rats in each group）. The rats were further stratified（n =6 each） by 0 h,1 d and 7 d after operation. Immunohistochemistry was used to detect the changes of Limk1 expression in the brain tissues. Results： The mean optical densities of Limk1 positive neuron in each group at different time spots were： 21. 658 ± 3. 990,30. 369 ± 5. 156 and 41. 546 ± 5. 677 in pure hypoxia-ischemia 0 h, 1 d and 7 d groups; 30. 261 ± 4. 266,43. 129 ± 5. 785 and 56. 309 ± 7. 198 in hypoxia preconditioned 0 h, 1 d and 7 d groups; 14. 113 ± 2. 983,16. 098 ± 3.116 and 15. 983 ± 3. 009 in the sham operation group 0 h, 1 d and 7 d groups. The mean optical density of Limk1 in both hypoxia preconditioned rats and pure hypoxia-ischemia rats was significantly higher than that in the sham operation group （ P 〈 0. 01 ）. The level of Limk1 expression in hypoxia preconditioned rats was significantly higher than that in the pure hypoxia-ischemia rats （ P 〈 0. 01 ）. The expression of Limk1 increased over time（0 h, 1 d,7 d） in both hypoxia preconditioned rats and pure hypoxia- ischemia rats after operation （ P 〈 0. 05 ）. Conclusion： The hypoxic preconditioning may up-regulate the expression of Limk1 in brain tissue of hypoxic-ischemic neonatal rat model, suggesting probable enhanced neural remodeling in the brain tissue of hypoxic-ischemic neonatal rats after hypoxic preconditioning.

关 键 词：缺血缺氧性脑病 LIMK1 树突棘 缺氧 大鼠 

分 类 号：R741[医药卫生—神经病学与精神病学]