[Electroacupuncture pretreatment alleviates post-stroke spasticity in rats by inhibiting NF-κB/NLRP3 signaling pathway-mediated inflammation and neuronal apoptosis].

X Sun, J Cai, A Zhang, B Pang, C Cheng, Q Cha, F Quan, T Ye
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Abstract

Objective: To explore the mechanism of electroacupuncture pretreatment (EP) for relieving post-stroke spasticity in rats.

Methods: 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.

Results: 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.

Conclusion: EP alleviates post-stroke spasticity in rats by inhibiting inflammatory responses and hippocampal neuronal apoptosis mediated by the NF-κB/NLRP3 signaling pathway.

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[电针预处理通过抑制NF-κB/NLRP3信号通路介导的炎症和神经元凋亡减轻大鼠脑卒中后痉挛]。
目的:探讨电针预处理(EP)缓解大鼠脑卒中后痉挛的作用机制。方法:将18只大鼠随机分为假手术组、大脑中动脉闭塞(MCAO)组和MCAO+EP组。MCAO+EP组大鼠在MCAO前连续3 d电针曲滨、百会穴。采用HE、Nissl和TUNEL染色检测大鼠的神经功能缺损和认知功能,并观察海马的病理变化。ELISA检测大鼠脑组织中IL-4、IL-6、TNF-α、TMAO的表达,qRT-PCR、Western blotting、免疫组化检测NF-κB p65、NLRP3、caspase-3、caspase-9 mRNA及蛋白表达水平。结果:MCAO大鼠神经功能缺损评分显著升高,海马肌张力升高,神经元凋亡数量增加,海马组织中IL-6、TNF-α、NF-κB p65、NLRP3、caspase-3、caspase-9表达增加,新物体识别时间明显缩短。显微镜下MCAO大鼠海马细胞排列不均松,细胞边界不清。I/R+EP组大鼠神经功能缺损评分和张力障碍评分明显降低,细胞凋亡减少,海马IL-6、TNF-α、caspase-3、caspase-9、NF-κB p65表达降低,新物体识别时间增加,海马细胞排列紧密、染色均匀,边界清晰,活跃神经元数量增加,IL-4表达增强。结论:EP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。
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来源期刊
南方医科大学学报杂志
南方医科大学学报杂志 Medicine-Medicine (all)
CiteScore
1.50
自引率
0.00%
发文量
208
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