Zhen ci yan jiu = Acupuncture research · 2026
[Effects of electroacupuncture on learning memory and central inflammatory response in rats with cerebral ischemia-reperfusion].
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Lu Zhuan, Chen Yu-Long, Wang Ya-Min, Liu Rui-Dong, Su Kai-Qi, Zhang Ming, Li Rui-Qing, Yin Shuai, Feng Xiao-Dong
Аннотация
OBJECTIVES: To observe the effects of electroacupuncture (EA) on learning memory and central inflammatory response in rats with middle cerebral artery occlusion/reperfusion (MCAO/R), and to explore its potential mechanisms.
METHODS: A total of 88 SD rats were randomly divided into a blank group (14 rats), a sham operation group (14 rats), and the remaining 60 rats were used to establish the MCAO/R model using the suture-occlusion method. The successfully modeled rats were randomly divided into a model group and an EA group, with 14 rats in each group. Rats of the EA group received EA at "Shenting" (GV24) and "Baihui" (GV20) for 30 min, once daily for 14 consecutive days. After intervention, neurological function and learning memory were evaluated using the Zea-Longa score and Morris water maze test. The brain infarction volume was assessed using TTC staining. Neuronal damage was observed using Nissl staining. Immunofluorescence was used to detect the positive expression of ionized calcium-binding adapter molecule 1 (Iba1) in the hippocampal CA1 region. ELISA was used to measure the levels of pro-inflammatory cytokines interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, and the blood-brain barrier-related factor S100β in serum. Western blot was used to detect the relative expression levels of Iba1, inflammatory factors, and tight junction proteins zonula occludens-1 (ZO-1), Occludin, and Claudin5 in the hippocampal tissue.
RESULTS: Compared with the sham operation group, rats of the model group showed increased neurological function scores (P<0.01), prolonged escape latency (P<0.01), reduced times of crossings over the original platform (P<0.01), increased brain infarction volume (P<0.001), abnormal hippocampal neuronal morphology, increased number of Iba1-labeled microglia (P<0.01), elevated relative expression level of Iba1 protein (P<0.01), increased protein expression levels of TLR4, NF-κB, IL-6, IL-1β and TNF-α in the hippocampal tissue (P<0.01), decreased protein expression levels of ZO-1, Occludin and Claudin5 (P<0.01), and increased contents of IL-6, IL-1β, TNF-α and S100β in serum (P<0.01). After EA intervention, compared with those of the model group, rats of the EA group showed decreased neurological function scores (P<0.01), shortened escape latency (P<0.01), increased times of crossings over the original platform (P<0.01), reduced brain infarction volume (P<0.01), more regular neuronal morphology, decreased number of Iba1-labeled microglia (P<0.01), decreased protein expression levels of TLR4, NF-κB, Iba1, IL-6, IL-1β, and TNF-α in the hippocampal tissue (P<0.01, P<0.05), increased protein expression levels of ZO-1, Occludin, and Claudin5 (P<0.01, P<0.05), and decreased contents of IL-6, IL-1β, TNF-α and S100β in serum (P<0.01).
CONCLUSIONS: EA at GV24 and GV20 can improve learning memory function in MCAO/R rats, and its mechanism may be related to the repair of the central blood-brain barrier, reduction of pro-inflammatory cytokine levels, and inhibition of microglial activation and central neuroinflammation.
METHODS: A total of 88 SD rats were randomly divided into a blank group (14 rats), a sham operation group (14 rats), and the remaining 60 rats were used to establish the MCAO/R model using the suture-occlusion method. The successfully modeled rats were randomly divided into a model group and an EA group, with 14 rats in each group. Rats of the EA group received EA at "Shenting" (GV24) and "Baihui" (GV20) for 30 min, once daily for 14 consecutive days. After intervention, neurological function and learning memory were evaluated using the Zea-Longa score and Morris water maze test. The brain infarction volume was assessed using TTC staining. Neuronal damage was observed using Nissl staining. Immunofluorescence was used to detect the positive expression of ionized calcium-binding adapter molecule 1 (Iba1) in the hippocampal CA1 region. ELISA was used to measure the levels of pro-inflammatory cytokines interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, and the blood-brain barrier-related factor S100β in serum. Western blot was used to detect the relative expression levels of Iba1, inflammatory factors, and tight junction proteins zonula occludens-1 (ZO-1), Occludin, and Claudin5 in the hippocampal tissue.
RESULTS: Compared with the sham operation group, rats of the model group showed increased neurological function scores (P<0.01), prolonged escape latency (P<0.01), reduced times of crossings over the original platform (P<0.01), increased brain infarction volume (P<0.001), abnormal hippocampal neuronal morphology, increased number of Iba1-labeled microglia (P<0.01), elevated relative expression level of Iba1 protein (P<0.01), increased protein expression levels of TLR4, NF-κB, IL-6, IL-1β and TNF-α in the hippocampal tissue (P<0.01), decreased protein expression levels of ZO-1, Occludin and Claudin5 (P<0.01), and increased contents of IL-6, IL-1β, TNF-α and S100β in serum (P<0.01). After EA intervention, compared with those of the model group, rats of the EA group showed decreased neurological function scores (P<0.01), shortened escape latency (P<0.01), increased times of crossings over the original platform (P<0.01), reduced brain infarction volume (P<0.01), more regular neuronal morphology, decreased number of Iba1-labeled microglia (P<0.01), decreased protein expression levels of TLR4, NF-κB, Iba1, IL-6, IL-1β, and TNF-α in the hippocampal tissue (P<0.01, P<0.05), increased protein expression levels of ZO-1, Occludin, and Claudin5 (P<0.01, P<0.05), and decreased contents of IL-6, IL-1β, TNF-α and S100β in serum (P<0.01).
CONCLUSIONS: EA at GV24 and GV20 can improve learning memory function in MCAO/R rats, and its mechanism may be related to the repair of the central blood-brain barrier, reduction of pro-inflammatory cytokine levels, and inhibition of microglial activation and central neuroinflammation.