摘要目的:探讨高压氧(HBO)对阿尔茨海默病(AD)模型大鼠认知功能及海马组织中脑源性神经营养因子(BDNF)、酪氨酸激酶受体B(TrkB)、神经生长因子(NGF)、突触素(SYN)表达水平的影响。方法:选取成年雄性SD大鼠80只，采用随机数字表法分为4组：正常对照组、假手术组、模型组和HBO组，每组20只。正常对照组未进行任何处理；假手术组每侧海马注射0.9%氯化钠溶液5 μl；模型组每侧海马注射β-淀粉样蛋白25-35(Aβ25-35)5 μl；HBO组每侧海马注射Aβ25-35 5 μl，注射2周后予以HBO干预。HBO干预结束后各组均行Morris水迷宫实验，检测各组大鼠学习与记忆能力及各组大鼠海马组织中BDNF、TrKB、NGF及SYN表达情况。结果:各组大鼠逃避潜伏期随着训练时间的延长而逐渐缩短，其中正常对照组与假手术组各时间点逃避潜伏期比较差异无统计学意义(均 P>0.05)，但第5、6天逃避潜伏期显著短于模型组(均 P<0.05)；HBO组第5、6天逃避潜伏期显著短于模型组(均 P<0.05)，但与正常对照组和假手术组比较差异无统计学意义(均 P>0.05)。正常对照组与假手术组原平台象限时间百分比、穿越原平台次数比较差异无统计学意义(均 P>0.05)，但显著多于模型组(均 P<0.05)；HBO组原平台象限时间百分比、穿越原平台次数显著多于模型组(均 P<0.05)，但与正常对照组和假手术组比较差异无统计学意义(均 P>0.05)。正常对照组与假手术组BDNF、TrkB、NGF蛋白相对表达量及SYN光密度比较差异均无统计学意义(均 P>0.05)，但显著高于模型组(均 P<0.05)；HBO组BDNF、TrkB、NGF蛋白相对表达量及SYN光密度显著高于模型组(均 P<0.05)，但与正常对照组和假手术组比较差异无统计学意义(均 P>0.05)。 结论:HBO可能通过上调与记忆密切相关的BDNF、TrkB、NGF和SYN表达，减轻AD模型大鼠认知障碍。

abstractsObjective:To investigate the effects of hyperbaric oxygen (HBO) on cognitive function and expression levels of brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B (TrkB), nerve growth factor (NGF), and synaptophysin (SYN) in hippocampal tissues of rat models with Alzheimer’s disease (AD).Methods:A total of 80 adult male SD rats were randomly divided into four groups: normal control group, sham operation group, model group, and HBO group, with 20 rats in each group. The normal control group did not receive any treatment; in the sham operation group, the hippocampus on each side of the rat brains was injected with 5 μl of 0.9% sodium chloride solution; in the model group, the hippocampus of rats was injected with 5 μl of β-amyloid 25-35 (Aβ25-35); and in the HBO group, the hippocampus of rats was also injected with 5 μl of Aβ25-35, which was given HBO intervention two weeks after the injection. After the HBO intervention, each group underwent Morris water maze experiment to detect the learning and memory ability of rats and the expressions of BDNF, TrKB, NGF, and SYN in their hippocampi.Results:The escape latency of rats in each group gradually shortened with the extension of training time. There was no significant difference in the escape latency between the normal control group and the sham operation group at each time point (all P>0.05), but on the 5th and 6th day, the escape latency in the HBO group was significantly shorter than that in the model group (all P<0.05), but there was no significant difference when the HBO group was compared with the normal control group or the sham operation group (all P>0.05). There was no significant difference between the normal control group and the sham operation group in the percentage of time spent in the original platform quadrant and the times of rats crossing the original platform (all P>0.05), but the percentage and the times in the two groups were both significantly higher than those in the model group (all P<0.05). The percentage of time spent in the original platform quadrant and the times of rats crossing the original platform in the HBO group were significantly higher than those in the model group (all P<0.05), but there was no significant difference when the HBO group was compared with the normal control group or the sham operation group (all P>0.05). The relative expressions of BDNF, TrkB, NGF protein, and SYN optical density in the normal control group were not significantly different from those in the sham operation group (all P>0.05), but they were significantly different from those in the model group (all P<0.05). The relative expressions of BDNF, TrkB, NGF protein, and SYN optical density in the HBO group were significantly higher than those in the model group (all P<0.05), but there was no significant difference when the HBO group was compared with the normal control group or the sham operation group (all P>0.05). Conclusion:HBO can alleviate the cognitive impairment of AD rat model by upregulating the expressions of BDNF, TrkB, NGF, and SYN, which are closely related to memory.