观察电针（EA）刺激“四神丛”（EX-HN1）和“风池”（GB20）对乳酸（Lac）含量、脯氨酸羟化酶2（PHD2）、缺氧诱导因子1α（HIF）表达的影响-1α)/核转录因子-κB(NF-κB)/NOD样受体热蛋白结构域相关蛋白3(NLRP3)信号通路以及血管性痴呆(VD)大鼠海马组织中的炎症因子,探讨Morris水迷宫试验筛选出的雄性SD大鼠随机分为空白对照组、假手术组、VD模型组和电针组(每组12只)。使用 4 血管闭塞 (VO) 方法复制 VD 模型。对 EX-HN1 和双侧 GB20 施加 EA（2 Hz，1 mA）30 分钟，每天一次，连续 21 天。采用Morris水迷宫试验检测造模前后及干预后大鼠的记忆学习能力。取海马组织样本，用H.E.观察组织病理学变化。染色；比色法检测Lac含量，ELISA法分别检测肿瘤坏死因子-α（TNF-α）、白细胞介素（IL）-1β、IL-18（血清中）的含量。采用免疫组化法检测海马组织中 PHD2、HIF-1α、p-NF-κB p65 的免疫活性水平,并检测 PHD2、HIF-1α、NF-κB p65、p-NF-κB p65、NLRP3 蛋白的表达水平与空白对照组和假手术组比较,逃避潜伏期、海马 Lac 含量、海马和血清中 TNF-α、IL-1β、IL-18 含量、 HIF-1α、p-NF-κB p65 免疫活性及 HIF-1α、NF-κB p65、p-NF-κB p65、NLRP3 蛋白表达水平显着升高（P<0.01），而原平台数模型组PHD2免疫活性和蛋白表达水平显着降低（P<0.05，P<0.01）。电针干预后，建模引起的上述指标的升高和降低在电针组均得到逆转（P<0.05，P<0.01）。他。染色结果显示模型组海马组织神经元排列紊乱、胞质染色不均匀、核仁模糊或核仁消失、毛细血管扩张、凋亡小体较多、炎性细胞增多，电针组有一定改善，包括电针刺激 EX-HN1 和 GB20 可改善 VD 大鼠的认知功能，这可能与其降低 Lac 含量、调节HIF-1α通路相关蛋白的表达，抑制海马组织的炎症反应。

To observe the effects of electroacupuncture (EA) stimulation of "Sishencong"(EX-HN1) and "Fengchi"(GB20) on lactate (Lac) content, expression of proline hydroxylase 2 (PHD2), hypoxia-inducible factor-1α (HIF-1α)/nuclear transcription factor- κB (NF- κB)/NOD-like receptor thermoprotein structural domain-associated protein 3 (NLRP3) signaling pathway, and inflammatory factors in hippocampal tissue of vascular dementia (VD) rats, so as to explore its mechanisms underlying improvement of VD.Male SD rats screened by Morris water maze tests were randomly divided into blank control, sham-operation, VD model and EA groups (12 rats in each group). The VD model was replicated using the 4-vessel occlusion (VO) method. EA (2 Hz, 1 mA) was applied to EX-HN1 and bilateral GB20 for 30 min, once daily for consecutive 21 days. Morris water maze test was employed to test the rat's memory learning ability before and after modeling and after the intervention. The hippocampal tissue was sampled for observing histopathologic changes with H.E. staining；and detecting Lac content with colorimetric method, and the contents of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-18 (also in serum) by using ELISA, respectively. The immunoactivity levels of PHD2, HIF-1α, and p-NF-κB p65 in hippocampal tissue were detected by immunohistochemistry, and the expression levels of PHD2, HIF-1α, NF-κB p65, p-NF-κB p65 and NLRP3 proteins in hippocampal tissue were detected by Western blot.Compared with the blank control and sham-operation groups, the escaping latency, Lac content in hippocampus, the TNF-α, IL-1β, and IL-18 contents in both hippocampus and serum, the immunoactivity of HIF-1α and p-NF-κB p65 and expression levels of HIF-1α, NF-κB p65, p-NF-κB p65, and NLRP3 proteins were significantly increased (P<0.01), while the number of original platform crossing, and PHD2 immunoactivity and protein expression level were significantly decreased (P<0.05, P<0.01) in the model group. Following EA intervention, modeling induced increase and decrease of the indexes mentioned above were all reversed in the EA group (P<0.05, P<0.01). H.E. staining showed disordered arrangement of neurons, uneven cytoplasm stain, blurred nucleolus or disappearance of nucleolus, dilated capillaries, many apoptotic bodies and increased inflammatory cells in the hippocampus tissue of the model group, which was improved to a certain extent in the EA group, including relatively regular arrangement of neurons, reduced apoptotic bodies and inflammatory cells, etc. in the hippocampus.EA stimulation of EX-HN1 and GB20 can improve the cognitive function in VD rats, which may be related to its functions in reducing Lac content, regulating the expression of HIF-1α pathway related proteins, and inhibiting inflammatory responses in the hippocampus tissue.