| 摘要: |
| 目的：探讨电针“风池”（GB20）与“神庭”（GV24）对血管性痴呆（vascular dementia，VD）大
鼠认知功能的影响，并分析其作用机制与调控核因子E2 相关因子2/ 谷胱甘肽过氧化物酶4（nuclear factor
erythroid-2 related factor 2/glutathione peroxidase 4，Nrf2/GPX4）信号通路、抑制铁死亡的相关性。方法：将46
只SD 雄性大鼠随机分为假手术组、模型组、电针组及电针+Nrf2 抑制剂组，采用双侧颈总动脉永久结扎法建
立VD 模型。电针组与电针+Nrf2 抑制剂组接受穴位电针干预，后者干预前腹腔注射ML385。通过Morris 水
迷宫实验评估认知功能；苏木素- 伊红（hematoxylin-eosin Staining，HE）染色与透射电镜观察海马结构；蛋
白质印迹法（western blot，WB）与免疫荧光技术（immunofluorescence，IF）检测Nrf2、GPX4 表达；测定谷胱甘
肽（glutathione，GSH）、丙二醛（malondialdehyde，MDA）与活性氧（reactive oxygen species，ROS）评估氧化应激
状态。结果：与假手术组相比，模型组大鼠逃避潜伏期延长，目标象限停留时间与穿越平台次数减少，海马神
经元排列紊乱、线粒体损伤明显，GSH 下降，MDA 与ROS 升高，Nrf2、GPX4 表达下调，差异均有统计学意义
（P <0.05 或P <0.01）。与模型组相比，电针组上述指标均显著改善（P <0.05，P <0.01），Nrf2 抑制剂可部分逆
转电针效应（P <0.05）。结论：电针“风池”“神庭”可改善VD大鼠认知功能，其机制可能与激活Nrf2/GPX4通路、
增强抗氧化能力、抑制铁死亡有关。 |
| 关键词: 电针 血管性痴呆 铁死亡 Nrf2/GPX4 信号通路 氧化应激 认知功能 大鼠 |
| DOI： |
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| Mechanism of action of electroacupuncture in improving rats with vascular dementia by activatingthe nuclear factor erythroid 2-related factor 2/glutathione peroxidase 4 signaling pathway andinhibiting ferroptosis |
| LIU Li,WANG Yan,MA Lifeng,MA Jianhua,WANG Xiaoli,SONG Andong |
| (Department of Traditional Chinese Medicine, The First People’s Hospital of Yinchuan, Yinchuan 750001,
Ningxia, China;;School of Traditional Chinese Medicine, Ningxia Medical University, Yinchuan 750001, Ningxia, China) |
| Abstract: |
| Objective: To investigate the effect of electroacupuncture （EA）at“Fengchi”（GB20）and
“Shenting”（GV24）on cognitive function in rats with vascular dementia （VD）, as well as its mechanism of action by
regulating the nuclear factor erythroid 2-related factor 2 （Nrf2）/glutathione peroxidase 4 （GPX4） signaling pathway
and inhibiting ferroptosis. Methods: A total of 46 male Sprague-Dawley rats were randomly divided into sham-operation
group, model group, EA group, and EA+Nrf2 inhibitor group, and permanent ligation of both common carotid arteries was
performed to establish a model of VD. The rats in the EA group and the EA+Nrf2 inhibitor group were given EA, and those
in the latter group were given intraperitoneal injection of ML385 before intervention. The Morris water maze test was used
to assess cognitive function; HE staining and transmission electron microscopy were used to observe hippocampal structure;
Western blot and immunofluorescence assay were used to measure the expression levels of Nrf2 and GPX4; glutathione
（GSH）, malondialdehyde （MDA）, and reactive oxygen species （ROS） were measured to assess oxidative stress
status. Results: Compared with the sham-operation group, the model group had a significant increase in escape latency
and significant reductions in the time spent in the target quadrant and the number of platform crossings, with disordered
arrangement of hippocampal neurons and obvious mitochondrial injury, as well as a significant reduction in GSH, significant
increases in MDA and ROS, and significant reductions in the expression levels of Nrf2 and GPX4（P < 0.05 or P < 0.01）.
Compared with the model group, the EA group had significant improvements in the above indicators（P < 0.05 or P < 0.01）,
and Nrf2 inhibitor partially reversed the effect of EA （P < 0.05）. Conclusion: EA at “Fengchi” and “Shenting” can
improve the cognitive function of VD rats, possibly by activating the Nrf2/GPX4 pathway, enhancing antioxidant capacity,
and inhibiting ferroptosis. |
| Key words: electroacupuncture vascular dementia ferroptosis nuclear factor erythroid 2-related factor 2/glutathione
peroxidase 4 signaling pathway oxidative stress cognitive function rats |
