Electroacupuncture attenuates middle cerebral artery occlusion-induced learning and memory impairment by regulating microglial polarization in hippocampus

被引:1
|
作者
Wen, Qiong [1 ,2 ]
Zha, Fubing [3 ]
Shan, Linlin [3 ]
Zhang, Shaohua [2 ]
Xiao, Peng [2 ]
Zhang, Chunxia [2 ]
Yu, Haibo [1 ]
Wang, Yulong [3 ]
机构
[1] Guangzhou Univ Chinese Med, Clin Med Coll 4, Shenzhen, Peoples R China
[2] Shenzhen Dapeng New Dist Nanao Peoples Hosp, Dept Rehabil, Shenzhen, Peoples R China
[3] Shenzhen Univ, Affiliated Hosp 1, Shenzhen Peoples Hosp 2, Dept Rehabil, Shenzhen, Peoples R China
关键词
Electroacupuncture; ischemic stroke; cognitive impairment; microglial polarization; neuroinflammation; ACTIVATED PROTEIN-KINASES; ISCHEMIC-STROKE; ISCHEMIA/REPERFUSION INJURY; COGNITIVE IMPAIRMENT; BRAIN-INJURY; ACUPUNCTURE; STIMULATION; MECHANISMS; EXPRESSION; RATS;
D O I
10.1080/00207454.2024.2313664
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
BackgroundAs a traditional medical therapy, electroacupuncture (EA) has been demonstrated to have beneficial effects on ischemic stroke-induced cognitive impairment. However, the underlying mechanism is largely unclear.MethodsAdult rats received occlusion of the middle cerebral artery and reperfusion (MCAO/R) to establish the ischemic stroke model. Morris water maze test was performed following EA stimulation at the GV20, PC6, and KI1 acupoints in rats to test the learning and memory ability. Western blot, immunofluorescent staining, and enzyme-linked immunosorbent assay were conducted to assess the cellular and molecular mechanisms.ResultsEA stimulation attenuated neurological deficits. In the Morris water maze test, EA treatment ameliorated the MCAO/R-induced learning and memory impairment. Moreover, we observed that MCAO/R induced microglial activation and polarization in the ischemic hippocampus, whereas, EA treatment dampened microglial activation and inhibited M1 microglial polarization but enhanced M2 microglial polarization. EA treatment inhibited the increased expression of proinflammatory cytokines and enhanced the increased expression of anti-inflammatory cytokines. Finally, we found that EA treatment dampened microglial p38 mitogen-activated protein kinase (MAPK) phosphorylation.ConclusionCollectively, our data suggested that EA treatment ameliorated cognitive impairment induced by MCAO/R and the underlying mechanism may be p38-mediated microglia polarization and neuroinflammation.
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页数:13
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