针药结合对阿尔茨海默病大鼠额叶皮质BDNF、SIRT1表达的影响

Changes of BDNF and SIRT1 expression in the frontal cortex of Alzheimer disease rats induced by electroacupuncture and gastrodin

目的:观察电针结合天麻素对阿尔茨海默病(AD)大鼠额叶皮质脑源性神经营养因子(BDNF)、沉默信息调节因子2同源蛋白1(SIRT1)的表达,探讨针药结合治疗AD的可能机制。方法:SD大鼠60只,随机分为6组:正常组、假手术组、模型组、电针组、天麻素组与针药结合组,每组10只。采用腹腔注射D-半乳糖与双侧海马注射β淀粉样蛋白1-40(Aβ1-40)复制AD大鼠模型。电针组电针刺激"百会"、"大椎"、双侧"足三里"穴,时间30 min,每天1次,共治疗4周;天麻素组腹腔注射天麻素注射液(10 mg/kg),每天1次,共治疗4周;针药结合组予以电针联合天麻素治疗,连续4周。免疫组织化学染色法检测各组大鼠额叶皮质BDNF、SIRT1的表达。结果:与正常组比较,假手术组大鼠额叶皮质BDNF、SIRT1的表达差异无统计学意义(P>0.05),模型组表达弱于正常组(P<0.05);电针组和天麻素组的表达强于模型组(P<0.05);针药结合组的表达强于电针组或天麻素组(P<0.05)。结论:电针与天麻素均能上调AD大鼠额叶皮质BDNF、SIRT1的表达,且两者结合的效果尤为显著,这可能是针药结合抗AD作用机制之一。

Objective ：To observe the changes of brain-derived neurotrophic factor（BDNF） and SIRT1 expression in the frontal cortex of Alzheimer disease （AD） rats induced by electroacupmmture（EA） and gastrodin for investigating the potential mechanisms of combined EA with medicine in treatment of AD. Methods：Sixty SD rats were randomized into normal groups of normal control,sham operation, models, EA intervention, gastrodin treatment and EA＋ gastrodin（ n- 10 for each group）. Rat models of AD were developed by intraperitoneal injection of D-galactose and bilateral injection of ARM-40 into the hippocampi. Rats in the EA group were stimulated at the points of Baihui,Dazhui and Zusanli,for 30 min,once a day,for 4 consecutive weeks, and ani- mals in the medication group were treated with gastrodin（ 100 mg/kg） once a day for 4 consecutive weeks. Rats in the EA＋ gastrodin group were managed with EA and gastrodin for 4 consecutive weeks. Then the expression of BDNF and SIRT1 in the frontal cortex of rats in each group was determined by im- munohistochemical staining. Results：BDNF and SIRT1 expression in the frontal cortex remained no significant difference in rats in the sham operation group as compared with that in the normal controls （P〉 0.05）. The expression of BDNF and SIRT1 was weaker in the model group than that in the normal control group （P〈 0.05）. Rats in the EA and gastrodin treatment groups had higher expression of BDNF and SIRT1 than the model group （P〈 0.05 ）, yet lower expression than the EA＋gastrodin group（P〈0.05）. Conclusion：Either EA or gastrodin could increase the expression of BDNF and SIRT1 in the frontal cortex in rats of AD,yet combined use of the EA and gastrodin may produce better effects on the expression of two genes,which may be one of the mechanisms against AD by stimulation and medication.