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电针对氯胺酮成瘾大鼠岛叶皮质中D1受体(D1R)表达、细胞外调节蛋白激酶1/2(p-ERK1/2)磷酸化及c-Fos的影响

Effects of Electroacupuncture on Expression of D1 Receptor (D1R), Phosphorylation of Extracellular-Regulated Protein Kinase 1/2 (p-ERK1/2), and c-Fos in the Insular Cortex of Ketamine-Addicted Rats.

作者信息

Wu Feng, Ding Jian, Li Huai-Bin, Miao Hua-Chun, Bao Rui, Yang Shan

机构信息

Department of Anatomy, Wannan Medical College, Wuhu, Anhui, China (mainland).

出版信息

Med Sci Monit Basic Res. 2019 Jan 31;25:26-32. doi: 10.12659/MSMBR.913285.

Abstract

BACKGROUND The aim of this study was to investigate the effects of electroacupuncture (EA) on expression of the D1 receptor (D1R), phosphorylation of extracellular-regulated protein kinase 1/2 (p-ERK1/2) and c-Fos in the insular cortex (IC) of ketamine-addicted rats. MATERIAL AND METHODS Sprague-Dawley rats were randomly divided into 7 groups: the normal group, the normal saline (NS) group, the ketamine (Ket) group, the U0126+Ket group, the SCH23390+Ket group, the Ket+acupoints EA (EA1) group, and the Ket+ non-acupoints EA (EA2) group. We used immunohistochemistry to detect the expression of D1R, p-ERK1/2, and c-Fos. We also used Nissl staining techniques to study the morphology of IC neurons. RESULTS Our study demonstrated that the ketamine group had sparsely distributed neurons, large intracellular vacuoles, nuclei shift, and unclear nucleolus. The number of Nissl-positive (neuronal) cells in the ketamine group were decreased than in the normal group. Our results also indicated that there was significantly lower expression of D1R, p-ERK1/2, and c-Fos in the IC of the U0126+Ket group, SCH23390+Ket group, and Ket+EA1 group as compared with that of the Ket group. CONCLUSIONS Ketamine addiction induces c-Fos overexpression in the IC by increasing the expression of D1R and p-ERK1/2. Acupoints EA downregulate D1R and p-ERK1/2 by reducing the overexpression of c-Fos.

摘要

背景 本研究旨在探讨电针(EA)对氯胺酮成瘾大鼠岛叶皮质(IC)中D1受体(D1R)表达、细胞外调节蛋白激酶1/2(p-ERK1/2)磷酸化及c-Fos的影响。

材料与方法 将Sprague-Dawley大鼠随机分为7组:正常组、生理盐水(NS)组、氯胺酮(Ket)组、U0126+Ket组、SCH23390+Ket组、Ket+穴位电针(EA1)组和Ket+非穴位电针(EA2)组。我们采用免疫组织化学法检测D1R、p-ERK1/2和c-Fos的表达。我们还使用尼氏染色技术研究IC神经元的形态。

结果 我们的研究表明,氯胺酮组神经元分布稀疏,细胞内有空泡,细胞核移位,核仁不清晰。氯胺酮组尼氏阳性(神经元)细胞数量比正常组减少。我们的结果还表明,与氯胺酮组相比,U0126+Ket组、SCH23390+Ket组和Ket+EA1组IC中D1R、p-ERK1/2和c-Fos的表达明显降低。

结论 氯胺酮成瘾通过增加D1R和p-ERK1/2的表达诱导IC中c-Fos过表达。穴位电针通过降低c-Fos的过表达下调D1R和p-ERK1/2。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1024/6369650/e672fa4f0101/medscimonitbasicres-25-26-g001.jpg

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