电针百会、四关穴对大鼠局灶性脑缺血再灌注大鼠大脑皮质中Tax1结合蛋白1表达的影响

发布时间：2019-08-06 08:48

【摘要】：目的观察电针百会、四关穴对大鼠局灶性脑缺血再灌注大鼠大脑皮质中Tax1结合蛋白1(TAX1BP1)表达的影响,探讨电针抑制核因子-κB(NF-κB)信号通路的激活,发挥脑保护作用的可能机制。方法 105只健康雄性Sprague-Dawley大鼠随机分为假手术组、模型组和电针组,每组再分为缺血2 h后再灌注6 h、12 h、24 h、48 h、72 h五个亚组。改良Longa线栓法制备右侧大脑中动脉梗死再灌注模型。电针组给予电针百会穴和病侧四关(合谷/太冲)穴。检测各组神经功能,缺血区大脑皮质中TAX1BP1蛋白的表达情况、TAX1BP1阳性细胞数、锌指蛋白A20和胞核NF-κB p65蛋白的表达情况。结果假手术组无神经功能缺损,与模型组相比,电针组在局灶性脑缺血2 h再灌注48 h、72 h时神经功能评分降低(P0.05)。与假手术组相比,模型组在再灌注12h、24 h、48 h时TAX1BP1蛋白表达增加(P0.05);与模型组相比,电针组在再灌注12 h、24 h、48 h、72 h时TAX1BP1蛋白表达进一步增加(P0.05),再灌注24 h为表达高峰。在再灌注24 h后,与假手术组相比,模型组A20表达、TAX1BP1阳性细胞数、胞核NF-κB p65表达增加(P0.05);与模型组相比,电针组的A20表达、TAX1BP1阳性细胞数进一步增加(P0.05),胞核NF-κB p65蛋白表达减少(P0.05)。免疫荧光结果显示,TAX1BP1蛋白主要表达在胞浆,电针组TAX1BP1与A20共表达在胞浆。免疫组化结果显示,模型组NF-κB p65主要表达在胞核,电针组主要表达在胞浆。结论电针抑制大鼠局灶性脑缺血再灌注后NF-κB信号通路的激活,促进大鼠神经功能恢复,其机制可能是通过上调TAX1BP1蛋白的表达,从而发挥脑保护作用。
[Abstract]:Objective to observe the effect of electro-acupuncture at Baihui and Siguan points on the expression of Tax1 binding protein 1 (TAX1BP1) in cerebral cortex of rats with focal cerebral ischemia and reperfusion, and to explore the possible mechanism of EA inhibiting the activation of nuclear factor-kappa B (NF-) signaling pathway and playing a protective role in the brain. Methods 105 healthy male Sprague-Dawley rats were randomly divided into sham operation group, model group and EA group. Each group was divided into 5 subgroups: ischemia 2 h, reperfusion 6 h, 12 h, 24 h, 48 h, 72 H 5 subgroup. The right middle cerebral artery infarction model was established by modified Longa suture method. The acupuncture group was given acupuncture at Baihui point and Siguan (Hegu / Taichong) point on the diseased side. The nerve function, the expression of TAX1BP1 protein in the cerebral cortex, the number of TAX1BP1 positive cells, the expression of zinc finger protein A20 and nuclear NF- 魏 B p65 protein were detected. Results there was no neurological deficit in the pseudo-operation group. Compared with the model group, the neurological function score of the electro-acupuncture group decreased at 72 hours after focal cerebral ischemia for 48 hours (P 0.05). Compared with the model group, the expression of TAX1BP1 protein in the model group increased at 12 h, 24 h and 48 h (P 0.05), and compared with the model group, the expression of TAX1BP1 protein increased further at 12 h, 24 h, 72 h and 24 h, respectively, and the expression of TAX1BP1 protein reached the peak at 24 h. After 24 hours of reperfusion, compared with the pseudo-operation group, the expression of A20, the number of TAX1BP1 positive cells and the expression of NF- 魏 B p65 in the nucleus increased in the model group (P 0.05). Compared with the model group, the expression of A20 and TAX1BP1 positive cells in the acupuncture group increased further (P 0.05), and the expression of NF- 魏 B p65 protein in the nucleus decreased (P 0.05). The results of immunofluorescence showed that TAX1BP1 protein was mainly expressed in cytoplasm, and TAX1BP1 and A20 were co-expressed in cytoplasm in EA group. The results of immunohistochemistry showed that NF- 魏 B p65 was mainly expressed in the nucleus in the model group and in the cytoplasm in the acupuncture group. Conclusion EA can inhibit the activation of NF- kappa B signaling pathway and promote the recovery of neural function in rats after focal cerebral ischemia and reperfusion. the mechanism may be to up-regulate the expression of TAX1BP1 protein and thus play a protective role in the brain.
【作者单位】：重庆医科大学附属第一医院神经内科;重庆市神经病学重点实验室;重庆医科大学附属第一医院中西医结合科;
【基金】：国家自然科学基金项目(No.30470606;No.81403243) 重庆市渝中区科技计划项目(No.20160102) 重庆市卫生局中医药科技项目(No.2012-2-128)
【分类号】：R245

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