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目的探讨大鼠幼年期轻型颅脑损伤(mild traumatic brain injury,mTBI)对成年期学习记忆功能的影响及其机制。方法将120只幼年期(4周龄)SD大鼠随机分为3组:正常组、假手术组和mTBI组,每组40只。应用液压冲击法制作大鼠mTBI模型。伤后1、4、8、12周,应用水迷宫试验检测大鼠学习记忆功能。伤后30 min、6 h、24 h、48 h、1周、4周、8周和12周,应用末端脱氧核糖核酸转移酶介导的粘性末端标记法(terminal deoxynucleoitidyl transferasemediated nick end labeling,TUNEL)染色和caspase-3免疫组化染色分析大鼠海马组织细胞凋亡,每组每个时间点5只大鼠。结果水迷宫试验结果显示,正常组大鼠和假手术组大鼠各年龄段的潜伏期差异均无统计学意义(P>0.05),mTBI组各年龄段的潜伏期均较假手术组明显延长(P<0.01)。正常组大鼠和假手术组大鼠海马组织可见少量TUNEL阳性和caspase-3阳性细胞,但是两组各时间点TUNEL阳性细胞和caspse-3阳性细胞差异均无统计学意义(P>0.05);mTBI组各时间点大鼠海马组织TUNEL阳性细胞和caspase-3阳性细胞均明显增多(P<0.01)。结论大鼠幼年期mTBI导致的认知功能损害是一个长期持续性的过程,与海马组织迟发性进行性神经元凋亡密切相关。
Objective To investigate the effect and mechanism of mild traumatic brain injury (mTBI) on learning and memory in adulthood. Methods 120 juvenile (4 weeks old) SD rats were randomly divided into 3 groups: normal group, sham operation group and mTBI group, 40 rats in each group. Rat model of mTBI was made by hydraulic impact method. At 1,4,8,12 weeks after injury, water maze test was used to detect learning and memory in rats. After 30min, 6h, 24h, 48h, 1week, 4week, 8weeks and 12weeks post-injury, terminal deoxynucleotidyl transferase nick end labeling (TUNEL) Staining and caspase-3 immunohistochemical staining of rat hippocampal tissue apoptosis, each group at each time point 5 rats. Results The results of water maze test showed that there was no significant difference in latency between rats in normal group and sham operation group (P> 0.05), and the incubation period in mTBI group was longer than that in sham operation group (P> <0.01). A small amount of TUNEL positive cells and caspase-3 positive cells were observed in hippocampus of rats in normal group and sham operation group, but there was no significant difference in TUNEL positive cells and caspse-3 positive cells between two groups at each time point (P> 0.05). The levels of TUNEL positive cells and caspase-3 positive cells in hippocampus of mTBI group were significantly increased at each time point (P <0.01). Conclusion The mTBI-induced cognitive impairment in the juvenile rats is a long-term persistent process, which is closely related to the delayed progressive neuronal apoptosis in the hippocampus.