Abstract:
This study aims to investigate how electroacupuncture regulates the learning and memory abilities of poststroke cognitive impairment (PSCI) rats through the TLR4/NF-κB/NLRP3 signaling pathway on the hippocampal microglia. Thirty male rats were randomly divided into three groups: sham surgery group, PSCI model group, and electroacupuncture group, with 10 rats in each group. Middle cerebral artery occlusion was used to establish the PSCI model. The Zea Longa method was used to score the rats\' neurological function. Electroacupuncture was utilized for 21 days to improve PSCI. The learning and memory abilities of rats were tested using the Morris water maze. Hematoxylin-eosin staining and immunofluorescence were used to find the hippocampus\' pathological changes. The concentration of interleukin-1β, interleukin-6, tumor necrosis factor-α, and interleukin-18 were detected by ELISA. The mRNA expression levels of associated inflammatory corpuscles were measured by quantitative real-time PCR. The protein expression levels of TLR4, MyD88, NF-κB, and NLRP3 were measured using western blotting. Electroacupuncture improved not only the learning and memory abilities of PSCI rats but also hippocampal morphology. Electroacupuncture inhibited the activation of microglia and the TLR4/NF-κB/NLRP3 signaling pathway. Electroacupuncture also reduced proinflammatory factors and restrained the mRNA levels of NLRP3-associated inflammatory cytokines. Its mechanism was related to inhibiting the expression of the TLR4/NF-κB/NLRP3 signaling pathway, attenuating the release of inflammatory factors, and regulating the activation of hippocampal microglia in the brain.
摘要:
本研究旨在探讨电针如何通过TLR4/NF-κB/NLRP3信号通路对脑卒中后认知功能障碍(PSCI)大鼠的学习记忆能力的影响。30只雄性大鼠随机分为3组:假手术组,PSCI模型组,和电针组,每组10只大鼠。采用大脑中动脉闭塞建立PSCI模型。采用ZeaLonga法对大鼠神经功能进行评分。使用电针21天以改善PSCI。使用Morris水迷宫测试大鼠的学习和记忆能力。苏木精-伊红染色和免疫荧光法发现海马病理变化。白细胞介素-1β的浓度,白细胞介素-6,肿瘤坏死因子-α,ELISA法检测白细胞介素-18。通过定量实时PCR测量相关炎症小体的mRNA表达水平。TLR4、MyD88、NF-κB的蛋白表达,和NLRP3使用蛋白质印迹法测量。电针不仅改善了PSCI大鼠的学习记忆能力,而且改善了海马形态。电针抑制小胶质细胞活化及TLR4/NF-κB/NLRP3信号通路。电针还可以降低促炎因子并抑制NLRP3相关炎症因子的mRNA水平。其机制与抑制TLR4/NF-κB/NLRP3信号通路的表达有关,减弱炎症因子的释放,调节大脑中海马小胶质细胞的激活。