| 刘 钊,车彦军,潘恩裕,陈 兴,庞陆军.颅脑损伤模型大鼠认知功能障碍及P-tau蛋白表达的研究[J].现代生物医学进展英文版,2017,17(8):1448-1451. |
| 颅脑损伤模型大鼠认知功能障碍及P-tau蛋白表达的研究 |
| The Study of Cognition Function Impairment and Expression of P-tau Protein in Rats with Traumatic Brain Injury |
| Received:August 31, 2016 Revised:September 26, 2016 |
| DOI：10.13241/j.cnki.pmb.2017.08.010 |
| 中文关键词: 颅脑损伤 认知功能障碍 P-tau蛋白 动态表达 |
| 英文关键词: Traumatic Brain Injury Cognition Function Impairment P-tau Protein Dynamic Expression |
| 基金项目: |
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| 中文摘要: |
| 摘要 目的：探讨颅脑损伤模型大鼠认知功能障碍及P-tau蛋白表达变化。方法：将60只Wistar大鼠随机分为假手术组和模型组，模型组根据时间点分为6 h、1 d、7 d和21 d，每组10只。采用改良的Feeney's自由落体装置制备大鼠颅脑损伤模型。损伤后6h、1d、7 d和21 d采用水迷宫法动态观察大鼠认知功能变化，Western blot检测大鼠海马组织P-tau蛋白表达。结果：模型组大鼠颅脑损伤6 h后，逃避潜伏期明显长于假手术组(P<0.05)，随损伤时间延长，其逃避潜伏期时间逐渐缩短，损伤后7 d逃避潜伏期仍高于假手术组(P<0.05)。在损伤同侧脑组织中，与假手术组比较，模型组大鼠损伤后6 h脑组织中P-Tau蛋白表达未见明显差异(P>0.05)，随损伤时间延长，P-Tau蛋白表达逐渐增多，且在损伤后7 d表达最高 (P<0.05)，21 d时减少(P<0.05)。在损伤对侧脑组织中，与假手术组比较，模型组大鼠损伤后6 h脑组织P-tau表达明显增高(P<0.05)，1 d时处于较高水平(P<0.05)，后逐渐减少，7 d，21 d时P-tau表达无差异(P>0.05)。结论：颅脑损伤可导致大鼠出现认知功能障碍，其损伤脑组织P-tau蛋白表达呈现先增加后减少趋势，且以损伤中后期表达明显。 |
| 英文摘要: |
| ABSTRACT Objective: To observe the study of cognition function impairment and expression of P-tau protein in rats with traumatic brain injury. Methods: 60 wistar rats were divided randomly into sham-operated and model groups, the last group were divided into 6 hour,1 day, 7day and 21 day group according to the sampling time, with 10 rats in each groups. Model of craniocerebral injury was duplicated by the metheds of Feeney's, the change of cognition function impairment was observed by Water maze test after 6 hour, 1 day,7 day and 21 days, the protein of p-tau was detected by western blot. Results: The escape latencies in model groups after 6 hours were extend than the sham-operated group(P<0.05), and with the injury, the escape latencies gradually shortened,and the time in 7 days after injury was higher than the sham-operated group(P<0.05). In the ipsilateral brain tissue, compare with the sham-operated group, the p-tau protein in model groups after 6 hours was undifferentiated(P>0.05), but with the injury, the p-tau protein were increased(P<0.05), and was highest after 7 days(P<0.05). In the contralateral brain tissue, compare with the sham-operated group,the p-tau protein in model groups after 6 hours was increased(P<0.05), and were decreased with the time(P<0.05), and was undifferentiated in 7 and 21 days(P>0.05). Conclusion: The cognition function impairment was exist in traumatic brain injury, and the protein of P-tau was climb up and then decline, and was obvious in the middle and later periods of the injuries. |
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