摘要
目的观察电针神庭、百会对局灶性脑缺血大鼠学习记忆能力的影响,以及海马组织病理学和核因子-κB p65(NF-κB-p65)及其抑制蛋白(IκB)mRNA表达的改变。方法线栓法制备局灶性脑缺血损伤大鼠模型。45只Sprague-Dawley大鼠随机分为假手术组、模型组、电针组,每组15只。电针组行电针干预14 d。14 d后行跳台测试;HE染色观察大鼠海马组织形态学;逆转录-PCR(RT-PCR)检测大鼠海马组织中NF-κB-p65和IκB mRNA水平。结果跳台实验显示,电针组大鼠在3 min内受到电击次数(2.2±0.94)次,较模型组的(7.60±2.67)次显著减少(P<0.001),电针组跳下平台的平均潜伏期(137.33±32.20)s,较模型组的(76.93±28.57)s显著延长(P<0.001)。电针组大鼠海马区域细胞损伤及NF-κB-p65 mRNA水平明显降低、IκB mRNA水平明显提高。结论抑制脑缺血海马组织中神经细胞的溶解及NF-κB-p65的活化,可能是电针改善局灶性脑缺血再灌注大鼠学习记忆能力的机制之一。
Objective To observe the effect of electroacupuncture at Shenting （DU24） and Baihui （DU20） on learning and memory abili- ty, as well as the finding of histopathology and the expression of mRNA of nuclear factor κB p65 （NF-κB-p65） and its inhibitor （IKB） in the hippocampus of rats with cerebral ischemia/reperfusion （I/R） injury. Methods 45 male Sprague-Dawley rats were were randomly diveded in- to sham control group （SC, n=15）, ischemia control group （IC, n=15） and electroacupuncture group （EA, n=15）. The latter 2 groups were modeled as focal cerebral I/R injury, and the EA group received electroacupuncture at Shenting （DU24） and Baihui （DU20） for 14 d. They were evaluated with the step down test, their hippocampus was observed under HE staining and the level of NF-κB-p65 and IicB mRNA was determined with RT-PCR 14 d after modeling. Results The frequence of shock was less, and the latency jumping down from the safe plat- form was longer in the EA group than in the IC group （P〈0.001）. The damage of the nerve cell and the expression ofNF-κB-p65 mRNA sig- nificantly decreased and the expression of InB mRNA increased in the EA group compared with those of IC group （P〈0.001）. Conclusion The inhibition of NF-kB-p65 might mediate the recovery of learning and memory impairment after electroacupuncture for cerebral ischemia.
出处
《中国康复理论与实践》
CSCD
北大核心
2013年第3期227-230,共4页
Chinese Journal of Rehabilitation Theory and Practice
基金
福建省科技厅重点项目(No.2010I0007)
科技部国际科技合作项目(No.2011DFG33240)
关键词
脑缺血
电针
学习记忆
核因子-ΚB
核因子-κB抑制蛋白
cerebral ischemia
electroacupuncture
learning and memory
nuclear factor KB
inhibitor of nuclear factor nB
