<?xml version="1.1" encoding="utf-8"?>
<article xsi:noNamespaceSchemaLocation="http://jats.nlm.nih.gov/publishing/1.1/xsd/JATS-journalpublishing1-mathml3.xsd" dtd-version="1.1" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"><front><journal-meta><journal-id journal-id-type="publisher-id">MRP</journal-id><journal-title-group><journal-title>Medical Research and Practice</journal-title></journal-title-group><issn>2993-9690</issn><eissn>2993-9704</eissn><publisher><publisher-name>Art and Technology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.61369/MRP.11893</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title>刺五加对大鼠尼古丁戒断焦虑样行为的调节作用</title><url>https://artdesignp.com/journal/MRP/2/12/10.61369/MRP.11893</url><author>许胜炜,李高歌,陈心语,陈依琳,徐东方,吴桐</author><pub-date pub-type="publication-year"><year>2024</year></pub-date><volume>2</volume><issue>12</issue><history><date date-type="pub"><published-time>2024-12-20</published-time></date></history><abstract>目的：探究刺五加对尼古丁戒断大鼠焦虑样行为的影响及其在杏仁核谷氨酸和GABA系统中的调节机制。方法：采用皮下注射方法建立SD大鼠尼古丁戒断模型。通过高架十字迷宫（EPM）和旷场实验（OFT）测试焦虑行为，检测血清皮质酮（CORT）及杏仁核中谷氨酸（Glu）、GABA的含量，测定相关基因表达。结果： 尼古丁戒断大鼠的焦虑样行为显著增加，表现为在EPM中开臂停留时间比例和进入次数比例降低，在OFT中中央区域活动距离和持续时间缩短；而刺五加干预组大鼠的焦虑样行为明显改善。ELISA结果显示，尼古丁戒断大鼠血清CORT水平显著升高，刺五加干预能抑制这种升高。在杏仁核中，尼古丁戒断显著增加了Glu的含量和谷氨酸受体（GluA1）的表达，同时降低了GABA的含量和GABA合成酶（GAD67）以及GABA受体（GABRA1）的表达；刺五加干预则通过降低Glu水平、上调GABA含量以及调节相关受体和转运体的表达，恢复了杏仁核中谷氨酸和GABA系统的平衡。结论：刺五加能够有效缓解尼古丁戒断大鼠的焦虑样行为，其机制可能与调节杏仁核谷氨酸和GABA系统的平衡有关，为抗焦虑治疗提供了新的实验依据和理论支持。</abstract><keywords>刺五加,尼古丁,戒断焦虑,杏仁核</keywords></article-meta></front><body/><back><ref-list><ref id="B1" content-type="article"><label>1</label><element-citation publication-type="journal"><p>[1]Chellian R, Behnood-Rod A, Bruijnzeel DM, et al.. Rodent models for nicotine withdrawal. J Psychopharmacol. 2021;35(10):1169-1187.[2]Wu B, Tao X, Liu C, et al. Vitamin D3 reduces hippocampal NR2A and anxiety in nicotine withdrawal mice. Transl Neurosci. 2021;12(1):273-281. Published 2021 Jan 1.[3]Kj&amp;aelig;rstad HL, Macoveanu J, Knudsen GM, et al. Neural responses during down-regulation of negative emotion in patients with recently diagnosed bipolar disorder and their unaffected relatives. Psychol Med. 2023;53(4):1254-1265.[4]Sun YH, Hu BW, Tan LH, et al. Posterior Basolateral Amygdala is a Critical Amygdaloid Area for Temporal Lobe Epilepsy. Adv Sci (Weinh). 2024;11(48):e2407525.[5]Pollack MH, Jensen JE, Simon NM, Kaufman RE, Renshaw PF. High-field MRS study of GABA, glutamate and glutamine in social anxiety disorder: response to treatment with levetiracetam. Prog Neuropsychopharmacol Biol Psychiatry. 2008;32(3):739-43.[6]赵容杰,王玉花,赵正林,等.刺五加对酒精戒断焦虑的作用及机制[J].牡丹江医学院学报,2021,42(03):32-36.[7]焦宇,李丽波,王玉花,等.薄荷精油对尼古丁戒断大鼠焦虑行为的治疗作用及其机制[J].齐齐哈尔医学院学报,2021,42(13):1105-1110.[8]Miyazaki S, Oikawa H, Takekoshi H, Hoshizaki M, Ogata M, Fujikawa T. Anxiolytic Effects of Acanthopanax senticosus HARMS Occur via Regulation of Autonomic Function and Activate Hippocampal BDNF⁻TrkB Signaling. Molecules. 2018 Dec 31;24(1):132.[9]Chang RS, Cerit H, Hye T, Durham EL, Aizley H, Boukezzi S, Haimovici F, Goldstein JM, Dillon DG, Pizzagalli DA, Holsen LM. Stress-induced alterations in HPA-axis reactivity and mesolimbic reward activation in individuals with emotional eating. Appetite. 2022 Jan 1;168:105707.[10]Wang Y, Wu LH, Hou F, et al. Mitochondrial calcium uniporter knockdown in hippocampal neurons alleviates anxious and depressive behavior in the 3XTG Alzheimer's disease mouse model. Brain Res. 1840:149060. doi:10.1016/j.brainres.2024.149060.</p><pub-id pub-id-type="doi"/></element-citation></ref></ref-list></back></article>
