Sun X, Cai J, Zhang A, Pang B, Cheng C, Cha Q, Quan F, Ye T
Department of Neurology, First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang 550001, China.
Department of Rehabilitation Medicine, First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang 550001, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2024 Nov 20;44(11):2102-2109. doi: 10.12122/j.issn.1673-4254.2024.11.06.
To explore the mechanism of electroacupuncture pretreatment (EP) for relieving post-stroke spasticity in rats.
Eighteen rats were randomized equally into sham-operated group, middle cerebral artery occlusion (MCAO) group, and MCAO+EP group. In MCAO+EP group, the rats received electroacupuncture at the acupoints Qubin and Baihui for 3 consecutive days prior to MCAO. Neurological deficits and cognitive function of the rats were evaluated, and pathologies in the hippocampus were examined using HE, Nissl, and TUNEL staining. The expressions of IL-4, IL-6, TNF-α, and TMAO in the brain tissues were detected with ELISA, and the mRNA and protein expression levels of NF-κB p65, NLRP3, caspase-3, and caspase-9 were determined with qRT-PCR, Western blotting, and immunohistochemistry.
The rats receiving MCAO had significantly increased neurological deficit scores and showed increased muscle tension, number of apoptotic neurons, and expressions of IL-6, TNF-α, NF-κB p65, NLRP3, caspase-3 and caspase-9 in the hippocampus and significantly reduced length of time for new object recognition. Microscopically, the cells in the hippocampus of the MCAO rats showed uneven and loosened arrangement and unclear cell boundaries. In contrast, the rats in I/R+EP group showed significantly lowered neurological deficit scores and dystonia rating scores, reduced cell apoptosis, lowered hippocampal expressions of IL-6, TNF-α, caspase-3, caspase-9, and NF-κB p65, increased time for new object recognition, tightly arranged and uniformly stained hippocampal cells with clear boundaries, with also an increased number of active neurons and enhanced expression of IL-4 in the hippocampus.
EP alleviates post-stroke spasticity in rats by inhibiting inflammatory responses and hippocampal neuronal apoptosis mediated by the NF-κB/NLRP3 signaling pathway.
探讨电针预处理（EP）减轻大鼠脑卒中后痉挛的机制。
将18只大鼠随机均分为假手术组、大脑中动脉闭塞（MCAO）组和MCAO+EP组。在MCAO+EP组中，大鼠在MCAO前连续3天接受曲鬓和百会穴电针治疗。评估大鼠的神经功能缺损和认知功能，并用苏木精-伊红（HE）、尼氏（Nissl）和TUNEL染色检查海马区的病理变化。用酶联免疫吸附测定（ELISA）法检测脑组织中白细胞介素-4（IL-4）、白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）和氧化三甲胺（TMAO）的表达，并用实时定量聚合酶链反应（qRT-PCR）、蛋白质免疫印迹法（Western blotting）和免疫组织化学法测定核因子-κB p65（NF-κB p65）、NOD样受体蛋白3（NLRP3）、半胱天冬酶-3（caspase-3）和半胱天冬酶-9（caspase-9）的mRNA和蛋白表达水平。
接受MCAO的大鼠神经功能缺损评分显著增加，肌肉张力升高，海马区凋亡神经元数量增加，IL-6、TNF-α、NF-κB p65、NLRP3、caspase-3和caspase-9表达增加，新物体识别时间显著缩短。显微镜下，MCAO大鼠海马区细胞排列不均且疏松，细胞边界不清。相比之下，缺血/再灌注+电针预处理（I/R+EP）组大鼠神经功能缺损评分和肌张力评分显著降低，细胞凋亡减少，海马区IL-6、TNF-α、caspase-3、caspase-9和NF-κB p65表达降低，新物体识别时间延长，海马区细胞排列紧密、染色均匀、边界清晰，海马区活跃神经元数量增加，IL-4表达增强。
电针预处理通过抑制NF-κB/NLRP3信号通路介导的炎症反应和海马神经元凋亡减轻大鼠脑卒中后痉挛。
