王志杰,王永超,杨敏,等.电针百会穴对次声暴露大鼠学习记忆能力及其钙调素依赖性蛋白激酶Ⅱ-Tau蛋白信号通路的影响[J].中华物理医学与康复杂志,2021,43(7):595-601
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| 电针百会穴对次声暴露大鼠学习记忆能力及其钙调素依赖性蛋白激酶Ⅱ-Tau蛋白信号通路的影响 |
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| DOI：10.3760/cma.j.issn.0254-1424.2021.07.004 |
| 中文关键词: 次声防护 学习记忆障碍 电针 百会穴 钙调依赖性蛋白激酶Ⅱ Tau蛋白 |
| 英文关键词: Infrasound protection Learning disorders Memory disorders Electroacupuncture Calmodulin kinase Tau protein |
| 基金项目:国家自然科学基金项目（31470825） |
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| 摘要点击次数: 2577 |
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| 中文摘要: |
| 目的 观察电针百会穴对次声暴露大鼠学习记忆能力及CaMKⅡ-Tau蛋白信号通路的影响，探讨电针百会穴防护次声性脑损害的作用机制。 方法 选取SD大鼠48只，采用随机数字表法将其分为空白组、次声组、百会组和非穴组，每组12只大鼠。空白组大鼠每日放置于无次声作用的次声仓中2 h，百会组、非穴组和次声组大鼠每日暴露于8 Hz、130 dB次声仓中2 h，连续7 d。百会组和非穴组大鼠在次声暴露结束后2 h内给予电针干预，其中百会组电针百会穴，非穴组电针非经非穴点，均每日1次，连续电针干预7 d；空白组和次声组给予与百会组和非穴组同样的方法抓取和固定，但不进行电针干预，亦为每日1次，每次7 d。干预6、7 d后，分别采用Morris水迷宫定位航行实验和空间探索实验检测4组大鼠的空间学习记忆能力。Morris水迷宫实验结束后，每组按随机数字表法选取6只大鼠，采用尼氏染色法观察4组大鼠海马区神经细胞的形态学改变；将4组剩余6只大鼠采用蛋白免疫印迹法（Western blot）检测其海马区磷酸化钙调依赖性蛋白激酶Ⅱ（P-CaMKⅡ）和磷酸化Tau蛋白（P-Tau）的表达，并进行组间比较。 结果 干预6 d和7 d后，次声组大鼠逃避潜伏期较空白组显著延长，平台象限时间比、平台象限路程比显著下降，穿越平台区域次数显著减少（P＜0.05）；与次声组比较，百会组大鼠逃避潜伏期显著缩短，平台象限时间比、平台象限路程比显著上升，穿越平台区域次数显著增多（P＜0.05）。干预7 d后，次声组大鼠海马区神经元损伤程度较空白组显著加重、神经元数量较空白组显著减少；与次声组比较，百会组大鼠海马区神经元损伤程度显著减轻、神经元数量显著增多。干预7 d后，次声组大鼠海马区P-CaMKⅡ和P-Tau蛋白水平分别为（0.735±0.094）和（0.873±0.089）较空白组显著增加（P＜0.05）；与次声组比较，百会组大鼠海马区P-CaMKⅡ和P-Tau蛋白水平显著下降（P＜0.05）。 结论 电针百会穴可以提高次声暴露大鼠的学习记忆能力，对次声性脑损害具有一定的防护作用，其机制可能与电针百会穴可通过降低海马区CaMKⅡ活性（磷酸化水平）抑制海马区Tau蛋白过度磷酸化，从而保护海马神经元有关。 |
| 英文摘要: |
| Objective To observe the effect of electroacupuncture at the Baihui acupoint on learning and memory ability and on the calmodulin kinase (CaMK)Ⅱ-Tau protein signal pathway in rats exposed to infrasound, and to explore its mechanism. Methods Forty-eight Sprague-Dawley rats were randomly divided into a blank group, an infrasound group, a Baihui group and a non-acupoint group, each of 12. The rats in the blank group were placed in an infrasound chamber without infrasound for 2 hours daily. Those in the other 3 groups were exposed to 8Hz, 130dB infrasound in the chamber for 2 hours daily for 7 consecutive days. The rats in the Baihui and non-acupoint groups were given electroacupuncture within 2 hours after the infrasound exposure at the Baihui acupoint or elsewhere respectively. The rats in the blank and infrasound groups were given the same grasping and fixation, but no electroacupuncture. On the 6th and 7th day of intervention, Morris water maze positioning and navigation experiments and spatial exploration experiments were used to quantify the rats′ spatial learning and memory ability. Nissl staining was used to observe any changes in the morphology of the neurons in the hippocampus of 6 rats in each group. The expression of phosphorylated calmodulin-dependent protein kinase II (P-CaMKⅡ) and phosphorylated Tau protein (P-Tau) in the hippocampus was also documented using western blotting. Results After 6 or 7 days the average escape latency of the rats in the infrasound group was significantly longer than the blank group′s average. Platform quadrant time and distance ratios and the number of times crossing the platform area were also significantly lower. Compared with the infrasound group, the average escape latency of the Baihui group was significantly shorter, with the platform quadrant time and distance ratios and the number of times crossing the platform area significantly higher. After 7 days, the damage to hippocampal neurons among the rats in the infrasound group was significantly aggravated and the number of neurons was reduced significantly compared with the blank group. Compared with the infrasound group, significantly fewer neurons in the hippocampus were damaged in the Baihui group and the number of neurons had increased significantly. After the intervention the levels of P-CaMKⅡand P-Tau protein in the infrasound group had increased significantly compared with the blank group, but those levels in the Baihui group were significantly lower, on average. Conclusion Electroacupuncture at the Baihui acupoint can improve the learning and memory ability of rats exposed to infrasound, and has some protective effect against infrasound brain damage. That may be due to its inhibiting Tau protein hyperphosphorylation in the hippocampus by reducing CaMKⅡ activity. |
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