Wang Zhifeng, Xi Yujiang, Lan Junfeng, Yang Jiao, Shi Ting, Xu Shuangfeng, Xing Liwei, Pan Pan, Wang Jian
The First Clinical Medical College, Yunnan University of Chinese Medicine, Kunming, China.
College of Acupuncture and Massage, Yunnan University of Chinese Medicine, Kunming, China.
Neuroreport. 2025 Jun 4;36(9):456-466. doi: 10.1097/WNR.0000000000002167. Epub 2025 May 14.
This study aimed to investigate the neuroprotective effects of electroacupuncture (EA) at the Baihui and Dazhui acupoints in a rat model of ischemia-reperfusion injury. Ninety-six male Sprague-Dawley rats were randomly assigned to four groups ( n = 24 per group): Sham, middle cerebral artery occlusion (MCAO), MCAO+EA, and MCAO+MCC950. The MCAO model was induced using filament embolization. Neurological function was assessed using Zea Longa scores on days 1 and 7 posttreatment, while cerebral infarction volume was measured using 2,3,5-triphenyltetrazolium chloride staining. Gene expression levels of NLRP3 and GSDMD were quantified by RT-qPCR, and protein expressions of NLRP3, GSDMD, caspase-1, IL-1β, and IL-18 were evaluated via Western blotting, immunohistochemistry, immunofluorescence staining, and ELISA. On day 1, compared with the MCAO group, the MCAO+EA and MCAO+MCC950 groups exhibited significantly reduced mRNA and protein expressions of NLRP3 and GSDMD ( P < 0.05), as well as decreased levels of caspase-1, IL-1β, and IL-18 ( P < 0.05). However, no significant differences were observed in neurological deficit scores or cerebral infarction volume. By day 7, both the MCAO+EA and MCAO+MCC950 groups showed significant improvements in neurological function ( P < 0.05), reductions in cerebral infarction volume ( P < 0.05), and further decreases in the expression of NLRP3, GSDMD, caspase-1, IL-1β, and IL-18 ( P < 0.05). EA at the Baihui and Dazhui acupoints alleviates neurological deficits in ischemic stroke rats by inhibiting the NLRP3/caspase-1 inflammatory pathway and reducing the expression of apoptosis-related proteins such as NLRP3, GSDMD, caspase-1, IL-1β, and IL-18.
本研究旨在探讨电针百会穴和大椎穴对缺血再灌注损伤大鼠模型的神经保护作用。将96只雄性Sprague-Dawley大鼠随机分为四组（每组n = 24）：假手术组、大脑中动脉闭塞（MCAO）组、MCAO+电针组和MCAO+MCC950组。采用线栓法制备MCAO模型。在治疗后第1天和第7天，使用Zea Longa评分评估神经功能，同时采用2,3,5-三苯基四氮唑氯化物染色法测量脑梗死体积。通过RT-qPCR定量NLRP3和GSDMD的基因表达水平，并通过蛋白质印迹法、免疫组织化学法、免疫荧光染色法和酶联免疫吸附测定法评估NLRP3、GSDMD、半胱天冬酶-1、白细胞介素-1β和白细胞介素-18的蛋白表达。在第1天，与MCAO组相比，MCAO+电针组和MCAO+MCC950组的NLRP3和GSDMD的mRNA和蛋白表达显著降低（P < 0.05），半胱天冬酶-1、白细胞介素-1β和白细胞介素-18水平也降低（P < 0.05）。然而，神经功能缺损评分或脑梗死体积无显著差异。到第7天，MCAO+电针组和MCAO+MCC950组的神经功能均有显著改善（P < 0.05），脑梗死体积减小（P < 0.05），NLRP3、GSDMD、半胱天冬酶-1、白细胞介素-1β和白细胞介素-18的表达进一步降低（P < 0.05）。电针百会穴和大椎穴可通过抑制NLRP3/半胱天冬酶-1炎症通路并降低NLRP3、GSDMD、半胱天冬酶-1、白细胞介素-1β和白细胞介素-18等凋亡相关蛋白的表达，减轻缺血性脑卒中大鼠的神经功能缺损。
