高压氧治疗对创伤性脑损伤大鼠认知功能的影响

关键词：高压氧  创伤性脑损伤  认知

Keywords:hyperbaric oxygen  cognitive function  traumatic brain injury

摘要：

      摘要 目的：观察高压氧治疗对脑损伤大鼠认知功能的影响及海马区CCL2及其受体CCR2的表达变化。 方法：75只成年雄性SD大鼠按数字表法随机分为假手术组（Sham组）、脑外伤组（TBI组）和高压氧治疗组（HBOT组），每组各25只。HBOT组和TBI组均采用Feeney自由落体法制作脑外伤模型，HBOT组每天进行HBO治疗；Sham组暴露硬脑膜不予打击。运用Morris水迷宫测试认知功能；荧光免疫双标检测海马CA1区CCL2和CCR2的表达。实时定量PCR测定损伤侧海马CCL2和CCR2mRNA的表达情况。 结果：Morris水迷宫测试结果显示，HBOT组高压氧治疗后7d、14d 和21d 平均潜伏期下降，同时穿越平台次数增多，与TBI组相比，差异均有显著性意义（P<0.05）；免疫荧光双染法检测显示，大鼠TBI后海马CA1区CCL2 主要表达在星形胶质细胞，CCR2主要表达在神经元；实时定量PCR显示，脑损伤后3—21d损伤侧海马CCL2 mRNA、CCR2 mRNA水平明显上升，差异有显著性意义；高压氧治疗后海马CCL2 mRNA明显下降，与TBI组相比，7d组、14d组及21d组差异有显著性意义（P<0.05）。高压氧治疗7d、14d后海马CCR2 mRNA明显下降，与TBI组相比，7d组及14d组差异有显著性意义（P<0.05）。 结论：HBO 治疗可以改善创伤性脑损伤大鼠认知功能，其机制可能与海马CCL2/CCR2表达下调有关。

Abstract:

      Abstract Objective：To investigate the effect of hyperbaric oxygen(HBO) on cognitive function recovery in rats following traumatic brain injury(TBI) and the expression of CCL2 and its receptor CCR2 in hippocampus. Method：Seventy-five adult male SD rats were randomly divided into sham surgical group (Sham group), traumatic brain injury group (TBI group) and hyperbaric oxygen therapy group (HBOT group), each consisting of 25 animals. Traumatic brain injury model was established with Feeney's free fall in the TBI group and the HBOT group. The HBOT group received HBO therapy daily every day. The animals in sham surgical group just exposed dura mater, but without free fall impact. Cognitive function was assessed by Morris water maze. The expression of CCL2 and CCR2 in hippocampal CA1 region was detected with immunofluorescence staining method, and real-time quantitative PCR was used to evaluated changes of the levels of CCL2 and CCR2 mRNA in hippocampus. Result：7d,14d and 21d after HBO therapy, escape latency decreased and the number of times crossing the platform increased for the animals in the HBOT group. Statistical significance could be noted, when they were compared with those of the TBI group. The expression of CCL2 in hippocampal CA1 region was detected mainly in astrocytes, CCR2 mainly in the neurons. CCL2 mRNA, CCR2 mRNA levels in hippocampus significantly increased 3—21 days after traumatic brain injury, the difference was statistically significant. CCL2 mRNA levels in the HBOT group significantly decreased after 1 week, 2 weeks and 3 weeks HBO therapy compared with the TBI group, CCR2 mRNA levels in the HBOT group significantly decreased after 1 week and 2 weeks HBO therapy compared with the TBI group. Conclusion：HBO therapy could promote the recovery of cognitive function in rats with traumatic brain injury, the possible mechanism might be associated with the decreases in CCL2/CCR2 levels in hippocampus.