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机构地区:[1]河南省中医药研究院药理实验室,河南郑州450004
出 处:《辽宁中医杂志》2009年第8期1427-1429,共3页Liaoning Journal of Traditional Chinese Medicine
基 金:国家自然科学基金资助项目(39270837);河南省自然科学基金资助项目(984021000)
摘 要:目的:研究电针对局灶性脑缺血再灌注大鼠神经细胞凋亡和相关基因表达的影响。方法:SD雄性大鼠随机分为假手术组、模型对照组、尼莫地平组、电针治疗组(左侧肩禺、外关、髀关、足三里)、非穴位对照组(左侧天泉与曲泽连线中点、曲泽与郗门中点、五里与阴胞连线中点和膝关与中都连线中点)。采用线拴法造成大鼠局灶性脑缺血再灌注模型(MCAO),分别于缺血后即刻、再灌注后即刻和再灌注后2h电针,共3次。末端脱氧核糖核酸介导生物素化脱氧尿嘧啶缺口末端标记(TUNEL)法测定海马凋亡神经细胞,免疫组织化学方法研究海马神经细胞caspase-3、Bcl-2和Bax基因表达。结果:与假手术组比较,MCAO大鼠海马凋亡细胞明显增加,caspase-3和Bax基因表达增强,Bcl-2/Bax比值显著降低;电针能明显降低MCAO大鼠海马TUNEL、caspase、Bax和Bcl-2阳性细胞数,Bcl-2/Bax比值显著升高。结论:电针可通过抑制神经细胞凋亡途径实现对脑缺血及缺血再灌注损伤的保护作用。Objective : To observe the effect of electroacupuncture(EA) on neuron apoptosis in hippocampus of rats with cerebral ischemia and reperfusion injury. Methods: Male SD rats were randomly divided into sham-operation group, model contral group,nimodipine group,EA group and non-acupoint contral group. The model of focal cerebral ischemia-reperfusion (MCAO) in rat was established by Longa's thread method. EA ( 10Hz , 1.5 - 3 V, duration of 0. 6ms) was applied to left" Jianyu" ( LI15 ), "Waiguan" ( TE5 ), etc. for EA group, and the mid-points between left" Tianquan" ( PC2 ) and "Quze" ( PC3 ), ( PC3 ) and "Ximen" (PG4) , etc. for non-acupoint contral group. Terminal deoxynucleotidyl Transferase Biotin-dUTP Nick End Labeling (TUNEL staining) was used to observe neuron apoptosis in hippocampus. The protein expression of caspase-3, Bcl-2 and Bax in hippocampus were detected by immunohistochemistry method. Results:Compared with sham-operation group, TUNEL positive cells and caspase-3, Bcl-2 and Bax immunoreative neurons in hippocampus increased significantly, the ratio of Bcl-2/Bax was decreased in MCAO model control group rats. EA could decrease significantly TUNEL positive cells and caspase-3, Bcl-2 and Bax immunoreative neurons in hippocampus and increased significantly the ratio of Bcl-2/Bax, compared with MCAO model control group( P 〈 0. 05 -0. 001 ). Conclusion:EA of commonly used acupoints can inhibite neuron apeptosis by ajusting the rate of apoptosis improving and inhibiting numbers in Bcl-2 family and decreasing proteinase action in caspase family.
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