【目的】 观察电针风池穴对脑梗死大鼠的治疗作用及机制。【方法】 将80只雄性SD大鼠随机分为正常组、模型组、电 针组（电针风池穴）和电针+ AS1517499 [信号转导及转录激活因子 6（STAT6）抑制剂]组（电针风池穴+腹腔注射 AS1517499）， 每组20只。除正常组，其他各组大鼠采用线栓法建立脑梗死模型。造模结束后，进行分组干预。干预结束后，观察大鼠神 经功能缺损程度，氯化三苯基四氮唑（TTC）染色法测定脑梗死面积，苏木精-伊红（HE）染色法观察脑组织病理变化，脱氧核 糖核苷酸末端转移酶介导的缺口末端标记（TUNEL）染色法测定脑细胞凋亡率，酶联免疫吸附分析（ELISA）检测脑组织白细胞 介素6（IL-6）、γ干扰素（IFN-γ）、白细胞介素4（IL-4）、转化生长因子β（TGF-β）水平，Western Blot法检测脑组织小胶质细 胞标志物离子钙结合接头分子 1（Iba-1）、CD86、CD206 以及 STAT6/核因子 κB（NF-κB）信号通路相关蛋白 STAT6、磷酸化 STAT6（p-STAT6）、过氧化物酶体增殖物激活受体 γ（PPAR-γ）、磷酸化核因子 κB p65（p-NF-κB p65）的蛋白表达水平。 【结果】 与正常组比较，电针组神经功能缺损评分、脑梗死面积、脑细胞凋亡率以及脑组织促炎症因子IL-6、IFN-γ水平显 著升高，抗炎因子IL-4、TGF-β水平显著降低，M1小胶质细胞标志物CD86以及信号通路相关蛋白 p-NF-κB p65表达水平 显著升高，M2小胶质细胞标志物 CD206以及信号通路相关蛋白 STAT6、p- STAT6、PPAR-γ表达水平显著下降，差异均有 统计学意义（P＜0.05）。与模型组比较，电针组神经功能缺损评分、脑梗死面积、脑细胞凋亡率以及脑组织促炎症因子IL-6、 IFN-γ水平显著降低，IL-4、TGF-β水平显著升高，CD86及p-NF-κB p65表达水平显著下降，CD206及STAT6、p- STAT6、 PPAR-γ表达水平显著上升，差异均有统计学意义（P＜0.05）。电针组的上述指标治疗效果均显著优于电针＋AS1517499组。 【结论】 电针风池穴可通过调节STAT6/NF-κB信号通路使M1型小胶质细胞向M2型转化，从而改善大鼠脑梗死。

Objective To investigate the therapeutic effects and mechanisms of electroacupuncture （EA） at Fengchi points （GB20） on cerebral infarction in rats. Methods The 80 male SD rats were randomized into normal group，model group，EA group （EA at Fengchi），and EA + AS1517499 group （EA at Fengchi + intraperitoneal STAT6 phosphorylation inhibitor），with 20 rats in each group. A cerebral infarction model was established via intraluminal filament occlusion in all groups except for the normal group. After intervention，the neurological deficit scores of the rats were assessed. The cerebral infarction area was measured using 2，3，5-triphenyltetrazolium chloride （TTC） staining. Histopathological alterations in brain tissue were observed via hematoxylin-eosin （HE） staining. The rate of brain cell apoptosis was determined using terminal deoxynucleotidyl transferase dUTP nick end labeling （TUNEL） staining. The levels of interleukin-6（IL-6），interferon-gamma （IFN-γ），interleukin-4（IL-4）， and transforming growth factor-beta （TGF- β） in brain tissue were detected by enzyme-linked immunosorbent assay （ELISA）. Western Blot was used to measure the protein expression of microglial markers （Iba-1，CD86， CD206） and STAT6/NF- κB pathway proteins （STAT6， p-STAT6， PPAR- γ， p-NF- κB p65）. Results Compared with the normal group，the neurological deficit score，cerebral infarction area，apoptosis rate of brain cells and the levels of pro-inflammatory factors IL-6 and IFN- γ in the brain tissue of the EA group were significantly increased，and the levels of anti-inflammatory factors IL-4 and TGF-β were significantly decreased， the expression levels of M1 microglia marker CD86 and signal pathway-related protein p-NF- κB p65 were significantly increased， and the expression levels of M2 microglia marker CD206 and signal pathway-related proteins STAT6， p-STAT6 and PPAR- γ were significantly decreased， and the differences were statistically significant （P＜0.05）. Compared with the model group，the neurological deficit score，cerebral infarction area， brain cell apoptosis rate and the levels of IL-6 and IFN-γ in the brain tissue of the EA group were significantly decreased，the levels of IL-4 and TGF-β were significantly increased，the expression levels of CD86 and p-NF- κB p65 were significantly decreased，and the expression levels of CD206，STAT6，p-STAT6 and PPAR-γ were significantly increased，with statistically significant differences （P＜0.05）. The therapeutic effects of the above indexes in the EA group were significantly superior to those in the EA + AS1517499 group. Conclusion EA at Fengchi points mitigates cerebral infarction by shifting microglial polarization from M1 to M2 via STAT6/NF-κB pathway modulation.

R285.5

广东省中医药局科研项目（编号：20231269）