Fang Jian-Qiao, Zhu Shu-Xiu, Zhang Ying, Wang Fang, Zhu Qing-Yan
Zhejiang University of Chinese Medicine, Hangzhou 310005, China.
Zhen Ci Yan Jiu. 2013 Feb;38(1):35-9.
To observe the effect of electroacupuncture (EA) intervention on expression of phosphorylated mitogen activated protein kinase-P 38 (p-P 38 MAPK) protein and Interleukin 1beta (IL-1beta)mRNA in the frontal lobe and hippocampus in Alzheimer's disease (AD) rats so as to explore its mechanisms underlying improvement of AD in clinic.
Thirty-two SD rats were equally and randomly divided into normal control (normal), sham-operation (sham), model and EA groups. AD model was established by microinjection of Abeta(1-40) (10 microg/microL, 1 microL) into bilateral Meynert nucleus (AP: 1. 4 mm, L: 3 mm, H: 7 mm) and validated by water maze tests. Rats of the sham group were treated by microinjection of the same dose of normal saline into the bilateral Meynert Nucleus. EA (1 mA, 2 Hz) was applied to bilateral "Baihui" (GV 20), "Taixi" (KI 3) and "Zusanli" (ST 36) for 15 min, once daily for 12 sessions. Expression levels of p-P 38 MAPK protein and IL-1beta mRNA in the hippocampus and frontal lobe tissues were detected by Western blot and RT-PCR, respectively.
In comparison with the normal group, the expression levels of p-P 38 MAPK protein and IL-1beta mRNA in the hippocampus and frontal lobe tissues were upregulated significantly in the model group (P < 0.01). After 12 sessions of EA intervention, the expression levels of both p-P 38 MAPK protein and IL-1beta mRNA were down-regulated significantly (P < 0.01, P < 0.05) in spite of being still higher than those of the normal group. No significant differences were found between the normal and sham groups in the expression levels of both p-P 38 MAPK protein and IL-1beta mRNA (P > 0.05).
EA intervention can reduce the over expression of both p-P 38 MAPK protein and IL-1beta mRNA in the hippocampus and frontal cortex in AD rats, suggesting an improvement of AD after EA intervention by restraining the inflammatory reaction.
观察电针干预对阿尔茨海默病(AD)大鼠额叶和海马中磷酸化丝裂原活化蛋白激酶 -P38(p-P38 MAPK)蛋白表达及白细胞介素 1β(IL-1β)mRNA 的影响,以探讨其临床改善 AD 的机制。
将 32 只 SD 大鼠平均随机分为正常对照组(正常组)、假手术组(假手术组)、模型组和电针组。通过向双侧 Meynert 核(前囟:1.4 mm,旁开:3 mm,深度:7 mm)微量注射 Aβ(1-40)(10 μg/μL,1 μL)建立 AD 模型,并通过水迷宫试验进行验证。假手术组大鼠通过向双侧 Meynert 核微量注射相同剂量的生理盐水进行处理。电针(1 mA,2 Hz)刺激双侧“百会”(GV 20)、“太溪”(KI 3)和“足三里”(ST 36)15 分钟,每日 1 次,共 12 次。分别采用 Western blot 和 RT-PCR 检测海马和额叶组织中 p-P38 MAPK 蛋白表达水平及 IL-1β mRNA 水平。
与正常组相比,模型组海马和额叶组织中 p-P38 MAPK 蛋白表达水平及 IL-1β mRNA 水平显著上调(P < 0.01)。电针干预 12 次后,p-P38 MAPK 蛋白表达水平及 IL-1β mRNA 水平均显著下调(P < 0.01,P < 0.05),但仍高于正常组。正常组和假手术组在 p-P38 MAPK 蛋白表达水平及 IL-1β mRNA 水平上均无显著差异(P > 0.05)。
电针干预可降低 AD 大鼠海马和额叶皮质中 p-P38 MAPK 蛋白表达及 IL-1β mRNA 的过度表达,提示电针干预通过抑制炎症反应改善 AD。