Hyeong-Min Kim, Hyun-Seok Jo, Eun-Jong Kim, Ji-Min Na, Hyeng-Kyu Park, Jae-Young Han, Ki-Hong Kim, Insung Choi, Min-Keun Song
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引用次数: 0
Abstract
Diffuse axonal injury (DAI) following sudden acceleration and deceleration can lead to cognitive function decline. Various treatments have been proposed. Repetitive transcranial magnetic stimulation (rTMS), a non-invasive stimulation technique, is a potential treatment for enhancing neuroplasticity in cases of brain injury. The therapeutic efficacy of rTMS on cognitive function remains unconfirmed. This study investigated the effects of rTMS and the underlying molecular biomechanisms using a rat model of DAI. Sprague-Dawley rats (n = 18) were randomly divided into two groups: one receiving rTMS after DAI and the other without brain stimulation. All rats were subjected to sudden acceleration and deceleration using a DAI modeling machine to induce damage. MRI was performed to confirm the DAI lesion. The experimental group received rTMS at a frequency of 1 Hz over the frontal cortex for 10 min daily for five days. To assess spatial memory, we conducted the Morris water maze (MWM) test one day post-brain damage and one day after the five-day intervention. A video tracking system recorded the escape latency. After post-MWM tests, all rats were euthanized, and their brain tissues, particularly from the hippocampus, were collected for immunohistochemistry and western blot analyses. The escape latency showed no difference on the MWM test after DAI, but a significant difference was observed after rTMS between the two groups. Immunohistochemistry and western blot analyses indicated increased expression of BDNF, VEGF, and MAP2 in the hippocampal brain tissue of the DAI-T group. In conclusion, rTMS improved cognitive function in the DAI rat model. The increased expression of BDNF, VEGF, and MAP2 in the DAI-T group supports the potential use of rTMS in treating cognitive impairments associated with DAI.
突然加速和减速后的弥漫性轴索损伤(DAI)会导致认知功能下降。目前已提出了多种治疗方法。重复经颅磁刺激(rTMS)是一种非侵入性刺激技术,是增强脑损伤病例神经可塑性的潜在治疗方法。经颅磁刺激对认知功能的疗效仍未得到证实。本研究使用 DAI 大鼠模型研究了经颅磁刺激的效果及其潜在的分子生物机制。Sprague-Dawley 大鼠(n = 18)被随机分为两组:一组在 DAI 后接受经颅磁刺激,另一组未接受脑刺激。所有大鼠均使用 DAI 模型机进行突然加速和减速,以诱发损伤。进行核磁共振成像以确认 DAI 损伤。实验组在额叶皮层接受频率为1赫兹的经颅磁刺激,每天10分钟,持续5天。为了评估空间记忆,我们在脑损伤后一天和五天干预后一天进行了莫里斯水迷宫(MWM)测试。视频跟踪系统记录了逃逸潜伏期。在莫里斯水迷宫测试后,所有大鼠均被安乐死,并收集其脑组织,尤其是海马区的脑组织,进行免疫组化和免疫印迹分析。在DAI后的MWM测试中,大鼠的逃逸潜伏期没有差异,但在经颅磁刺激后,两组大鼠的逃逸潜伏期有显著差异。免疫组化和 Western 印迹分析表明,DAI-T 组海马脑组织中 BDNF、VEGF 和 MAP2 的表达增加。总之,经颅磁刺激改善了 DAI 大鼠模型的认知功能。在 DAI-T 组中,BDNF、VEGF 和 MAP2 的表达增加,这支持了经颅磁刺激在治疗与 DAI 相关的认知障碍方面的潜在用途。