目的：探究电针对缺血性脑卒中（CIS）大鼠的神经保护作用及其与 NLRP3/Caspase-1 炎症通路介导
的细胞焦亡的关联机制。方法：将48只SPF 级SD大鼠随机分为假手术组、大脑中动脉栓塞（MCAO）模型
组、电针组及抑制剂（MCC950）组，每组12只。采用改良 Zea-Longa 法构建大鼠脑缺血再灌注模型，电针组
于建模后第1天进行电针干预，每日1次，持续 14 d；抑制剂组同期给予腹腔注射 MCC950（3 mg/kg），每日1
次，持续14 d；假手术组与模型组不予干预。通过Zea Longa 5分制神经功能评分评估神经功能缺损程度，
TTC染色检测脑梗死体积，尼氏染色观察神经元存活状态，结合免疫组化、免疫荧光、实时荧光定量 PCR
（qPCR）、酶联免疫吸附试验（Elisa）及 Western blot（WB）技术，检测脑组织中 NLRP3、GSDMD 及下游 Cas
pase-1、IL-1β、IL-18 的mRNA与蛋白表达水平。结果：与假手术组相比，模型组大鼠神经功能缺损评分显著
升高（P＜0.001），脑梗死体积明显增大（P＜0.001），尼氏小体数量减少且神经元形态受损，NLRP3、GSD
MD、Caspase-1、IL-1β、IL-18的mRNA及蛋白表达均显著上调（P＜0.01或P＜0.001）。与模型组相比，电针
组与抑制剂组上述指标均显著改善：神经功能评分降低（P＜0.05或P＜0.001），脑梗死体积缩小（P＜0.001），
尼氏小体数量增多且神经元形态更完整（P＜0.001），NLRP3、GSDMD 及其下游炎症因子的mRNA与蛋白
表达水平均显著下降（P＜0.05、P＜0.01或P＜0.001）；且电针组与抑制剂组间各项指标无统计学差异（P＞
0.05）。结论：电针可通过抑制NLRP3/Caspase-1 炎症通路的激活，下调细胞焦亡相关蛋白（NLRP3、GSD
MD）及下游促炎因子（Caspase-1、IL-1β、IL-18）的表达，减轻脑缺血再灌注后的神经炎性损伤，缩小脑梗死
体积并改善神经功能，其神经保护作用与NLRP3抑制剂干预效果相当。
To explore the neuroprotective effect of electroacupuncture on cerebral ischemic stroke
(CIS) in rats and its associated mechanism with cell pyroptosis mediated by the NLRP3/Caspase-1 inflammatory
pathway. Methods: A total of 48 SPF-grade SD rats were randomly divided into four groups: the
sham-operation group, the middle cerebral artery occlusion (MCAO) model group, the electroacupuncture group,
and the inhibitor (MCC950) group, with 12 rats in each group. A rat cerebral ischemia-reperfusion model was
established using the modified Zea-Longa method. The electroacupuncture group received electroacupuncture
intervention starting on the first day after modeling, once a day for 14 days. The inhibitor group was
administered an intraperitoneal injection of MCC950 (3 mg/kg) during the same period, once a day for 14 days.
The sham-operation group and the model group received no intervention. The degree of neurological deficit was
evaluated using the Zea Longa 5-point neurological function score. The cerebral infarction volume was detected
by TTC staining, and the survival status of neurons was observed by Nissl staining. The mRNA and protein
expression levels of NLRP3, GSDMD, and their downstream Caspase-1, IL-1β, and IL-18 in brain tissue were
detected using immunohistochemistry, immunofluorescence, real-time fluorescent quantitative PCR (qPCR),
enzyme-linked immunosorbent assay (Elisa), and Western blot (WB) techniques. Results: Compared with the
sham-operation group, the neurological deficit score of rats in the model group was significantly increased (P<
0.001), the cerebral infarction volume was significantly enlarged (P<0.001), the number of Nissl bodies
decreased, and neuronal morphology was damaged. The mRNA and protein expressions of NLRP3, GSDMD,
Caspase-1, IL-1β, and IL-18 were all significantly upregulated (P<0.01 or P<0.001). Compared with the model
group, the above indicators in the electroacupuncture group and the inhibitor group were significantly improved:
the neurological function score decreased (P<0.05 or P<0.001), the cerebral infarction volume decreased (P<
0.001), the number of Nissl bodies increased, and neuronal morphology was more intact (P<0.001). The mRNA
and protein expression levels of NLRP3, GSDMD, and their downstream inflammatory factors were significantly
decreased (P<0.05, P<0.01, or P<0.001). Moreover, there were no statistical differences in the various indicators between the
electroacupuncture group and the inhibitor group (P>0.05). Conclusion: Electroacupuncture can inhibit the activation of the NLRP3/
Caspase-1 inflammatory pathway, downregulate the expression of cell pyroptosis-related proteins (NLRP3, GSDMD) and downstream
pro-inflammatory factors (Caspase-1, IL-1 β, IL-18), reduce neuroinflammatory damage after cerebral ischemia-reperfusion, decrease
cerebral infarction volume, and improve neurological function. Its neuroprotective effect is comparable to that of NLRP3 inhibitor
intervention.
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