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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。
Objective: To investigate the changes of cognitive dysfunction and P-tau protein expression in brain injury model rats. Methods: Sixty Wistar rats were randomly divided into sham operation group and model group. The model group was divided into 6 h, 1 d, 7 d and 21 d according to the time point, with 10 in each group. A modified model of Feeney’s free-fall device was used to establish the model of traumatic brain injury in rats. The changes of cognitive function in rats were observed by water maze at 6h, 1d, 7d and 21d after injury, and the expression of P-tau in hippocampus was detected by Western blot. Results: After 6 hours of traumatic brain injury, the escape latency of model group was significantly longer than that of sham-operation group (P <0.05). With the prolongation of injury time, the escape latency of model group was gradually shortened, and the escape latency of model group was still higher than that of sham operation group (P <0.05). Compared with the sham group, there was no significant difference in the expression of P-Tau protein in the ipsilateral 6 h after injury in model group (P> 0.05). With the prolongation of injury time, the expression of P-Tau protein (P <0.05), and decreased at 21 d (P <0.05). Compared with the sham-operation group, the expression of P-tau in the model group was significantly increased 6 h after injury (P <0.05), higher at 1 d (P <0.05) and later There was no difference in P-tau expression on day 7 and day 21 (P> 0.05). Conclusion: Craniocerebral injury can lead to cognitive dysfunction in rats. The expression of P-tau protein in the lesioned brain tissue first increased and then decreased, and the expression of P-tau protein was obvious in the middle and late stage of injury.