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目的研究硫胺素缺乏(TD)对成年小鼠认知功能及其海马神经发生的影响。方法TD 小鼠模型按照 TD 处理时间分为 TD 7、9、14、16、25 d 组和正常对照组,每组4～6只小鼠。Y 型迷宫检测学习记忆能力,5-溴脱氧尿嘧啶核苷(BrdU)体内掺入及 Doublecortin(Dcx)等免疫组化染色检测海马齿状回颗粒下层(DGSG)神经发生。结果在无病理损害及胆碱能神经变性的 TD 9 d 组,小鼠学会正确反应的总训练次数(22.3±2.2)与对照组(13.5±3.5)相比差异有统计学意义,而海马DGSG BrdU 标记的阳性细胞数(个/DGSG)19.8±0.4及 Dcx 标记免疫活性(像素/mm~2)1537.2±50.2也较对照组(分别为23.9±0.3和2688.9±127.9)显著降低。此时补充硫胺素可上调 BrdU 阳性细胞数(个/DGSG)23.6±1.9及 Dcx 免疫活性(像素/mm~2)2052.3±269.6,并减少其学会正确反应的训练总次数(16.8±0.5)。结论在病理损害前期,TD 导致的学习功能障碍可能与海马神经发生功能下调有关。
Objective To investigate the effects of thiamine deficiency (TD) on cognitive function and hippocampal neurogenesis in adult mice. Methods The TD mouse model was divided into TD 7, 9, 14, 16 and 25 d groups and normal control group with 4 to 6 mice in each group. Y-type maze test learning and memory ability, BrdU in vivo incorporation and Doublecortin (Dcx) and other immunohistochemical staining detection of hippocampal dentate gyrus granulomagica (DGSG) neurogenesis. Results In the TD 9 d group without pathological damage and cholinergic neurodegeneration, the total number of training sessions (22.3 ± 2.2) in mice that received the correct response was significantly different from that in the control group (13.5 ± 3.5), while the DGSG BrdU-labeled positive cells (a / DGSG) 19.8 ± 0.4 and Dcx labeled immunoreactivity (pixels / mm ~ 2) 1537.2 ± 50.2 also significantly lower than the control group (23.9 ± 0.3 and 2688.9 ± 127.9 respectively). At this point, thiamine supplementation could up-regulate the number of BrdU-positive cells (a / DGSG) at 23.6 ± 1.9 and Dcx immunocompetence (pixels / mm ~ 2) at 2052.3 ± 269.6 and reduce the total number of training sessions (16.8 ± 0.5) . Conclusion In the early stage of pathological damage, TD-induced learning dysfunction may be related to the down-regulation of hippocampal neurogenesis.