Rehabilitation Medicine, Qujing No.1 Hospital, Qujing, Yunnan, China.
Department of Neurology, Luoping County People's Hospital, Luoping, Yunnan, China.
Neurol Res. 2024 Jun;46(6):525-537. doi: 10.1080/01616412.2024.2337517. Epub 2024 Apr 2.
Vascular dementia (VD) is the second most common type of dementia worldwide. Previous studies have proven that transcranial direct current stimulation (tDCS) has potential applications in relieving cognitive impairment in VD animal models. The purpose of this study was to probe the mechanism by which tDCS combined with swimming exercise improves the learning and memory abilities of VD model rats.
The VD rat model was induced using the permanent bilateral common carotid artery occlusion (2-VO) method; tDCS was applied to the rats and then they took part in swimming exercises. Rat memory, platform crossing time, and platform crossing frequency were analyzed via a water maze experiment. Nerve damage in the cortex and hippocampal CA1 area of the rats was observed using Nissl staining. Western blotting, immunohistochemistry, immunofluorescence staining and reverse transcription quantitative polymerase chain reaction (RT - qPCR) were used to determine the expression of related proteins and genes. The levels of oxidative stress were detected by kits.
We demonstrated that VD model rats treated with tDCS combined with swimming exercise exhibited significant improvement in memory, and VD model rats exhibited significantly reduced neuronal loss in the hippocampus, and reduced microglial activation and M1 polarization. tDCS combined with swimming exercise protects VD model rats from oxidative stress through the miR-223-3p/protein arginine methyltransferase 8 (PRMT8) axis and inhibits the activation of the TLR4/NF-κB signaling pathway.
Our results suggest that tDCS combined with swimming exercise improved the learning and memory ability of VD model rats by regulating the expression of PRMT8 through miR-223-3p to affect microglial activation and M1 polarization.
血管性痴呆(VD)是全球第二常见的痴呆类型。先前的研究已经证明,经颅直流电刺激(tDCS)在缓解 VD 动物模型的认知障碍方面具有潜在的应用价值。本研究旨在探讨 tDCS 联合游泳运动改善 VD 模型大鼠学习记忆能力的机制。
采用永久性双侧颈总动脉闭塞(2-VO)法诱导 VD 大鼠模型;对大鼠进行 tDCS 处理,然后让它们参加游泳运动。通过水迷宫实验分析大鼠的记忆、平台穿越时间和平台穿越频率。采用尼氏染色观察大鼠皮质和海马 CA1 区的神经损伤。采用 Western blot、免疫组织化学、免疫荧光染色和逆转录定量聚合酶链反应(RT-qPCR)检测相关蛋白和基因的表达。试剂盒检测氧化应激水平。
我们证明,接受 tDCS 联合游泳运动治疗的 VD 模型大鼠的记忆能力显著改善,并且 VD 模型大鼠的海马神经元丢失明显减少,小胶质细胞激活和 M1 极化减少。tDCS 联合游泳运动通过 miR-223-3p/精氨酸甲基转移酶 8(PRMT8)轴保护 VD 模型大鼠免受氧化应激,并抑制 TLR4/NF-κB 信号通路的激活。
我们的研究结果表明,tDCS 联合游泳运动通过调节 PRMT8 的表达,通过 miR-223-3p 影响小胶质细胞的激活和 M1 极化,改善了 VD 模型大鼠的学习记忆能力。