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目的观察电针对阿尔茨海默病(AD)模型大鼠认知功能的影响及可能的作用机制。方法LETO大鼠8只为正常组;胰岛素抵抗OLETF大鼠23只采用腹腔注射D-半乳糖和灌胃Al Cl3溶液的方法建立AD模型后,随机分为模型组12只和电针组11只。电针组给予电针干预,连续3周,模型组与正常组无干预。干预结束后,采用Morris水迷宫实验观察各组大鼠行为学变化,检测各组大鼠空腹血糖(FPG)、血浆胰岛素(FINS)、血清C肽水平,计算胰岛素抵抗指数(HOMA-IR),并检测各组大鼠海马组织中的β-淀粉样蛋白(Aβ)及tau蛋白含量。结果 Morris水迷宫实验中,与模型组比较,电针组各时间定位航行实验的逃避潜伏期均显著缩短,空间探索实验的穿越平台象限时间延长(P<0.01)。与正常组比较,模型组大鼠FPG、FINS、HOMA-IR、C肽及海马Aβ和tau蛋白含量含量较正常组显著升高(P<0.01);与模型组比较,电针组大鼠海马FPG、FINS、HOMA-IR、C肽及海马Aβ和tau蛋白肽含量均降低(P<0.01)。结论电针可改善AD模型大鼠认知行为功能及脑AD样病理改变,其机制可能与改善期胰岛素抵抗状态有关。
Objective To observe the effect of electroacupuncture on cognitive function in Alzheimer’s disease (AD) model rats and its possible mechanism. Methods Twenty-three LETO rats were selected as the normal control group. Twenty-three insulin resistance OLETF rats were randomly divided into model group (n = 12) and EA group (n = 11) by intraperitoneal injection of D-galactose . Electroacupuncture group was given electroacupuncture for 3 consecutive weeks, the model group and the normal group without intervention. Morris water maze test was used to observe the behavioral changes of the rats in each group after the intervention. The levels of fasting blood glucose (FPG), plasma insulin (FINS) and serum C-peptide of the rats in each group were measured to calculate the insulin resistance index (HOMA-IR) The levels of β-amyloid protein (Aβ) and tau in hippocampus of rats in each group were measured. Results In the Morris water maze test, compared with the model group, the escape latency of electro-acupuncture at each time-oriented navigation experiment was significantly shortened, and the time of space exploration experiment was extended across the platform quadrant (P <0.01). Compared with the normal group, the content of FPG, FINS, HOMA-IR, C peptide and Aβ and tau in the hippocampus in model group were significantly higher than those in normal group (P <0.01). Compared with model group, The levels of Aβ and tau peptides in FPG, FINS, HOMA-IR, C-peptide and hippocampus decreased (P <0.01). Conclusion Electroacupuncture can improve the cognitive function of AD model rats and brain AD-like pathological changes, the mechanism may be related to the improvement of insulin resistance status.