He Chao, Yuan Ai-Hong, Yang Jun, Fan Yin-Qiu, Xie Hong-Yu
Graduate School of Anhui University of Chinese Medicine, Hefei 230038, China.
The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei 230031.
Zhen Ci Yan Jiu. 2022 Jun 25;47(6):485-90. doi: 10.13702/j.1000-0607.20210707.
To observe the effect of electroacupuncture(EA) on the expression of nuclear transcription factors κB (NF-κB) and Tau protein and content of amyloid (Aβ) in diabetic rats with cognitive impairment, so as to explore its mechanism underlying improvement of learning-memory ability.
Male SD rats were randomly divided into normal control (=9), model (=9) and EA (=9) groups. The diabetic mellitus model was established by feeding the rats with high fat and high sugar for 1 month and intraperitoneal injection of STZ (25 mg·kg-1·d-1) for 2 days. EA was applied to "Zusanli"(ST36) and "Neiting"(ST44) for 20 min, alternatively on both side every day, and "Yishu"(EX-B3) was stimulated by twirling the acupuncture needle with uniform reinforcing-reducing method for 1 min, followed by retaining it for 20 min. The treatment was conducted 6 times a week for 4 weeks. The learning-memory ability was evaluated by using Morris water maze swimming test. The blood glucose level was randomly detected by using a glucometer, the content of Aβ1-42 in the hippocampal tissue was detected by ELISA, and the relative expression levels of hippocampal Tau and NF-κB p65 proteins and mRNAs were determined by Western blot and fluorescence quantitative real-time PCR, separately.
After modeling, the blood glucose, escape latency, Aβ1-42 content and the expression levels of Tau and NF-κB p65 proteins and mRNAs in the model group were significantly increased (<0.01, <0.05) in comparison with the normal control group. Following EA intervention, the modeling induced increase of blood glucose, escape latency, Aβ1-42 content and the expression levels of Tau and NF-κB p65 proteins and mRNAs were reversed (<0.05, <0.01).
EA can improve the learning-memory ability in rats with diabetic cognitive impairment, which may be related to its function in down-regulating the levels of hippocampal Aβ1-42, Tau and NF-κB proteins.
观察电针（EA）对糖尿病认知功能障碍大鼠核转录因子κB（NF-κB）、Tau蛋白表达及淀粉样蛋白（Aβ）含量的影响，以探讨其改善学习记忆能力的机制。
雄性SD大鼠随机分为正常对照组（n = 9）、模型组（n = 9）和电针组（n = 9）。通过高脂高糖喂养大鼠1个月并腹腔注射链脲佐菌素（STZ，25 mg·kg-1·d-1）2天建立糖尿病模型。电针“足三里”（ST36）和“内庭”（ST44），交替双侧进行，每次20分钟，每天1次，用提插补泻法捻转针具刺激“胰俞”（EX-B3）1分钟，留针20分钟。每周治疗6次，共4周。采用Morris水迷宫游泳试验评估学习记忆能力。随机用血糖仪检测血糖水平，用ELISA法检测海马组织中Aβ1-42含量，分别用Western blot法和荧光定量实时PCR法检测海马Tau和NF-κB p65蛋白及mRNA的相对表达水平。
造模后，模型组血糖、逃避潜伏期、Aβ1-42含量及Tau和NF-κB p65蛋白及mRNA表达水平较正常对照组显著升高（P < 0.01，P < 0.05）。电针干预后，造模引起的血糖、逃避潜伏期、Aβ1-42含量及Tau和NF-κB p65蛋白及mRNA表达水平升高得到逆转（P < 0.05，P < 0.01）。
电针可改善糖尿病认知功能障碍大鼠的学习记忆能力，这可能与其下调海马Aβ1-42、Tau和NF-κB蛋白水平的作用有关。
