首页> 外文期刊>CNS neuroscience & therapeutics >Electroacupuncture protected pyramidal cells in hippocampal CA1 region of vascular dementia rats by inhibiting the expression of p53 and Noxa.
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Electroacupuncture protected pyramidal cells in hippocampal CA1 region of vascular dementia rats by inhibiting the expression of p53 and Noxa.

机译:电针对血管性痴呆大鼠海马CA1区锥体细胞的保护作用是抑制p53和Noxa的表达。

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AIM: Clinically electroacupuncture (EA) is proved an effective therapy for vascular dementia (VD), but their mechanisms remain uncertain. The aim of this study was to determine whether EA protects pyramidal cells from apoptosis in hippocampus of a VD rat model by inhibiting the expression of p53 and Noxa. METHODS: One month after a VD animal model was established by bilateral occlusion of common carotid arteries, EA treatment was given at "Baihui" (DU20), "Dazhui" (DU14), and "Shenshu" (BL23). The learning and memory ability was assessed by Morris water maze. Neuronal apoptosis in hippocampus was evaluated with hematoxylin-eosin (HE) staining, and the expression of p53 and Noxa was analyzed by confocal laser scanning microscope with immunofluorescence staining. RESULTS: Expressions of p53 and Noxa in the EA group and sham-operated group were less than in the VD model group (P < 0.01), and the expression of p53 was positively correlated to expression of Noxa in hippocampus of VD rats (r = 0.918, P < 0.01). EA treatment could reduce the amount of apoptotic neurons in hippocampal CA1 area of rats with VD. The average latency in the Morris water maze test was significantly shorter, and escape strategies improved from edge and random searches to more linear swim pathway in the EA group compared with the VD model group (P < 0.01). CONCLUSIONS: The increasing expressions of p53 and Noxa play important roles in the pathogenesis of VD. EA improves learning and memory ability and protects pyramidal cells from apoptosis by blocking expression of p53 and Noxa in the hippocampal CA1 region of VD rats. These results suggest a novel mechanism of EA treatment to VD.
机译:目的:临床上证明电针(EA)是治疗血管性痴呆(VD)的有效方法,但其作用机理尚不确定。这项研究的目的是确定EA是否通过抑制p53和Noxa的表达来保护VD大鼠模型海马的锥体细胞免于凋亡。方法:通过双侧闭塞颈总动脉建立VD动物模型一个月后,分别在“百会”(DU20),“大椎”(DU14)和“神树”(BL23)进行EA治疗。通过莫里斯水迷宫评估学习和记忆能力。用苏木精-伊红(HE)染色评估海马神经元凋亡,并用免疫荧光染色共聚焦激光扫描显微镜分析p53和Noxa的表达。结果:EA组和假手术组p53和Noxa的表达均低于VD模型组(P <0.01),p53的表达与VD大鼠海马中Noxa的表达呈正相关(r = 0.918,P <0.01)。 EA治疗可以减少VD大鼠海马CA1区的凋亡神经元。与VD模型组相比,EA组的Morris水迷宫测试中的平均潜伏期显着缩短,逃脱策略从边缘搜索和随机搜索改善为更多的线性游泳路径(P <0.01)。结论:p53和Noxa表达的增加在VD的发病中起重要作用。 EA通过阻止VD大鼠海马CA1区p53和Noxa的表达,提高学习和记忆能力,保护锥体细胞免于凋亡。这些结果表明EA治疗VD的新机制。

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