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1. 湖北中医学院
2. 华中科技大学同济医学院,武汉,430061
3. ,武汉,430061
纸质出版日期:2006
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孔立红, 孙国杰, 刘胜洪. 针刺对脑缺血再灌注大鼠海马组织核转录因子-κB表达及含量的影响[J]. 针刺研究, 2006,(3):140-144.
KONG Li-hong, SUN Guo-jie, LIU Sheng-hong. Effects of Acupuncture on the Expression and Content of Nuclear Factor-κB in Hippocampus of Rats with Cerebral Ischemia/Reperfusion[J]. Acupuncture research, 2006, (3): 140-144.
孔立红, 孙国杰, 刘胜洪. 针刺对脑缺血再灌注大鼠海马组织核转录因子-κB表达及含量的影响[J]. 针刺研究, 2006,(3):140-144. DOI:
KONG Li-hong, SUN Guo-jie, LIU Sheng-hong. Effects of Acupuncture on the Expression and Content of Nuclear Factor-κB in Hippocampus of Rats with Cerebral Ischemia/Reperfusion[J]. Acupuncture research, 2006, (3): 140-144. DOI:
目的:观察电针对脑缺血再灌注大鼠核转录因子-κB(NF-κB)信号分子表达和含量的影响
探讨针刺抗局灶性脑缺血再灌注损伤的神经细胞信号转导机制。方法:将120只SD大鼠随机分为正常组、假手术组、模型24h组、模型48h组、模型72h组、电针治疗24h组、电针治疗48h组、电针治疗72h组。采用改良线栓法制备局灶性脑缺血(MCAO)再灌模型
电针“大椎”、双侧“内关”穴(连续波
频率120次/min
强度1mA
持续30min)。运用免疫组化检测法和蛋白免疫印迹法
检测海马组织NF-κB-p65核转录因子蛋白的表达与含量。结果:模型各组大鼠缺血侧海马CA1区NF-κB-p65蛋白表达显著高于正常组和假手术组(P<0·05)
也显著高于电针治疗同时相各组(P<0·01)
NF-κB移位于核明显;模型各组大鼠缺血侧海马组织NF-κB-p65蛋白含量比电针治疗同时相各组高
有显著性差异(P<0·05)。结论:电针能下调脑缺血再灌注海马组织NF-κB蛋白水平
阻滞其转位于核
发挥神经保护作用。
Objective: To investigate the effects of electroacupuncture (EA) on the expression and content of nuclear factor-κB in hippocampus of rats with cerebral ischemia/reperfusion (CI/R). Methods: A total of 120 SD rats were randomly divided into normal group (n=10)
sham operation group (n=27)
model group (n=36) and EA group (n=36)
and the lateral 3 groups were evenly divided into 24 h
48 h and 72 h subgroups. CI/R model was established by middle cerebral artery occlusion(MCAO)and reperfusion with the suture in MCA. EA ( 2 Hz
1 mA
continuous waves) was applied to “Dazhui”(GV 14) and bilateral “Neiguan”(PC 6) for 30 min
once 3 h after CI/R
followed by once every 12 h . The hippocampus tissue was taken out to be cut into sections ( 5 μm ). The expression and content of nuclear factor (NF)-κB-p65 protein in hippocampus were assayed by immunohistochemistry and Western blotting. Results: In comparison with normal group
NF-κB-p65 expression-positive cells of hippocampal CA1 area in 24 h of model group
and every 48 h and 72 h subgroup of model and EA groups were significantly more ( P< 0.05
0.01). Compared with 24 h
48 h and 72 h subgroups of model group
NF-κB-p65 expression-positive cells in the corresponding subgroups of EA group were significantly fewer (P<0.01). The grey values of NF-κB-p65 protein in the 3 subgroups of model group were significantly higher than those of normal group and sham-operation groups (P<0.01); while the grey values of NF-κB-p65 in the 3 subgroups of EA group were markedly lower than those in the corresponding 3 subgroups of model group (P<0.05). Conclusion: EA can reduce the expression and content of nuclear factor-κB-p65 in hippocampus of rats with CI/R and prevent it from being transported to the nucleus of the neurons in hippocampal CA1 area
which may contribute to the protective effect of EA on ischemic neurons.
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