研究发现高频重复经颅磁刺激（HF-rTMS）可以改善认知障碍。然而，HF-rTMS对慢性脑灌注不足（CCH）的影响仍不清楚。旨在研究HF-rTMS对CCH小鼠认知改善的影响及其潜在机制。双侧颈动脉狭窄（BCAS）后每日进行HF-rTMS治疗）并持续14天。将小鼠随机分为三组：假手术组、模型组和 HF-rTMS 组。 Y 迷宫和新的物体识别测试用于评估认知功能。通过免疫荧光染色和蛋白质印迹分析MAP-2、突触、髓鞘碱性蛋白（MBP）和脑源性生长因子（BDNF）的表达，以评估神经元可塑性和白质髓鞘再生。尼氏染色及caspase-3、Bax、Bcl-2表达观察神经元凋亡情况。此外，通过荧光染色评估小胶质细胞和星形胶质细胞的活化。通过qPCR检测各组小鼠海马IL-1β、IL-6和肿瘤坏死因子(TNF)-α的炎症水平。通过行为测试，BCAS小鼠表现出新对象偏好率降低和降低了自发交替率，而 HF-rTMS 显着改善了海马学习和记忆缺陷。此外，模型组小鼠的 MAP-2、突触、MBP 和 BDNF 水平降低，而 HF-rTMS 治疗逆转了这些影响。正如预期的那样，模型组中活化的小胶质细胞和星形胶质细胞增加，但 HF-rTMS 治疗抑制了这些变化。 HF-rTMS 减少 BCAS 诱导的神经元凋亡和促凋亡蛋白（Caspase-3 和 Bax）的表达，并增加抗凋亡蛋白（Bcl-2）的表达。此外，HF-rTMS还能抑制炎症细胞因子（IL-1β、IL-6和TNF-α）的表达。HF-rTMS通过增强神经元可塑性和抑制炎症来减轻CCH小鼠的认知障碍，是一种潜在的方法用于血管性认知障碍。© 2024 作者。 《大脑与行为》由 Wiley periodicals LLC 出版。

High-frequency repetitive transcranial magnetic stimulation (HF-rTMS) has been found to ameliorate cognitive impairment. However, the effects of HF-rTMS remain unknown in chronic cerebral hypoperfusion (CCH).To investigate the effects of HF-rTMS on cognitive improvement and its potential mechanisms in CCH mice.Daily HF-rTMS therapy was delivered after bilateral carotid stenosis (BCAS) and continued for 14 days. The mice were randomly assigned to three groups: the sham group, the model group, and the HF-rTMS group. The Y maze and the new object recognition test were used to assess cognitive function. The expressions of MAP-2, synapsis, Myelin basic protein(MBP), and brain-derived growth factors (BDNF) were analyzed by immunofluorescence staining and western blot to evaluate neuronal plasticity and white matter myelin regeneration. Nissl staining and the expression of caspase-3, Bax, and Bcl-2 were used to observe neuronal apoptosis. In addition, the activation of microglia and astrocytes were evaluated by fluorescence staining. The inflammation levels of IL-1β, IL-6, and Tumor Necrosis Factor(TNF)-α were detected by qPCR in the hippocampus of mice in each group.Via behavioral tests, the BCAS mice showed reduced a rate of new object preference and decreased a rate of spontaneous alternations, while HF-rTMS significantly improved hippocampal learning and memory deficits. In addition, the mice in the model group showed decreased levels of MAP-2, synapsis, MBP, and BDNF, while HF-rTMS treatment reversed these effects. As expected, activated microglia and astrocytes increased in the model group, but HF-rTMS treatment suppressed these changes. HF-rTMS decreased BCAS-induced neuronal apoptosis and the expression of pro-apoptotic protein (Caspase-3 and Bax) and increased the expression of anti-apoptotic protein (Bcl-2). In addition, HF-rTMS inhibited the expression of inflammatory cytokines (IL-1β, IL-6, and TNF-α).HF-rTMS alleviates cognitive impairment in CCH mice by enhancing neuronal plasticity and inhibiting inflammation, thus serving as a potential method for vascular cognitive impairment.© 2024 The Author(s). Brain and Behavior published by Wiley Periodicals LLC.