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Article(id=1199335056792712008, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1199335049175859209, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.1157.2022.1006, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1652976000000, receivedDateStr=2022-05-20, revisedDate=null, revisedDateStr=null, acceptedDate=1663430400000, acceptedDateStr=2022-09-18, onlineDate=1763873360106, onlineDateStr=2025-11-23, pubDate=1711555200000, pubDateStr=2024-03-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1763873360106, onlineIssueDateStr=2025-11-23, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1763873360106, creator=13701087609, updateTime=1763873360106, updator=13701087609, issue=Issue{id=1199335049175859209, tenantId=1146029695717560320, journalId=1189873630562394117, year='2024', volume='49', issue='3', pageStart='245', pageEnd='366', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1763873358291, creator=13701087609, updateTime=1763874044185, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1199337926086721596, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1199335049175859209, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1199337926086721597, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1199335049175859209, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=343, endPage=348, ext={EN=ArticleExt(id=1199335057325388636, articleId=1199335056792712008, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Research progress on the effect of α7 nicotinic acetylcholine receptor on perioperative neurocognitive function, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

α7 nicotinic acetylcholine receptor (α7nAChR) is widely expressed in the central nervous system and immune system, and plays a neuro-immunoregulatory role. On the one hand, α7nAChR is involved in the transmission of neurotransmitters, the conduction of excitatory signals and the maintenance of synaptic plasticity, which is of great significance for maintaining the normal and stable neurocognitive function. On the other hand, as an important part of the cholinergic anti-inflammatory pathway, α7nAChR is involved in the regulation of physiological and pathological processes such as inflammatory response, oxidative stress, apoptosis and autophagy in the central system, and plays an immunomodulatory and neuroprotective role, thus being potential target for improving perioperative neurocognitive function. This article reviews the biological characteristics of α7nAChR and its effect on perioperative neurocognitive function, in order to provide ideas and methods for clinical improvement of perioperative neurocognitive function in surgical patients.

, correspAuthors=Dong-Bin Zhang, authorNote=null, correspAuthorsNote=
Email:
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α7烟碱型乙酰胆碱受体(α7nAChR)在中枢神经系统和免疫系统中广泛表达，发挥神经-免疫调节作用。一方面，α7nAChR参与神经递质的传递、兴奋性信号的传导和突触可塑性的维持，对于保持神经认知功能的正常与稳定具有重要意义；另一方面，α7nAChR作为胆碱能抗炎通路的重要组成部分，参与调节中枢系统炎症反应、氧化应激、细胞凋亡和自噬等生理、病理过程，发挥免疫调节和神经保护作用，是改善围手术期神经认知功能的潜在靶点。本文对α7nAChR的生物学特征及其对围手术期神经认知功能的影响进行综述，以期为临床改善手术患者的围手术期神经认知功能提供新的思路和方法。

, correspAuthors=张栋斌, authorNote=null, correspAuthorsNote=
张栋斌，E-mail：
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司尚坤，硕士研究生，主要从事中西医结合麻醉方面的研究

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司尚坤，硕士研究生，主要从事中西医结合麻醉方面的研究

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司尚坤，硕士研究生，主要从事中西医结合麻醉方面的研究

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α7烟碱型乙酰胆碱受体对围手术期神经认知功能的影响研究进展
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司尚坤 1 , 徐迎雪 2 , 张维亮 2 , 季加富 2 , 张栋斌 2, *
解放军医学杂志 | 综述 2024,49(3): 343-348
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解放军医学杂志 | 综述 2024, 49(3): 343-348
α7烟碱型乙酰胆碱受体对围手术期神经认知功能的影响研究进展
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司尚坤1, 徐迎雪2, 张维亮2, 季加富2, 张栋斌2, *
作者信息
  • 1山东中医药大学中医学院，山东济南 250014
  • 2山东中医药大学附属医院麻醉科，山东济南 250014

    • 司尚坤，硕士研究生，主要从事中西医结合麻醉方面的研究

通讯作者:

张栋斌，E-mail：
Research progress on the effect of α7 nicotinic acetylcholine receptor on perioperative neurocognitive function
Shang-Kun Si1, Ying-Xue Xu2, Wei-Liang Zhang2, Jia-Fu Ji2, Dong-Bin Zhang2, *
Affiliations
  • 1College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250014, China
  • 2Department of Anesthesiology, the Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250014, China
出版时间: 2024-03-28 doi: 10.11855/j.issn.0577-7402.1157.2022.1006
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摘要
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α7烟碱型乙酰胆碱受体(α7nAChR)在中枢神经系统和免疫系统中广泛表达，发挥神经-免疫调节作用。一方面，α7nAChR参与神经递质的传递、兴奋性信号的传导和突触可塑性的维持，对于保持神经认知功能的正常与稳定具有重要意义；另一方面，α7nAChR作为胆碱能抗炎通路的重要组成部分，参与调节中枢系统炎症反应、氧化应激、细胞凋亡和自噬等生理、病理过程，发挥免疫调节和神经保护作用，是改善围手术期神经认知功能的潜在靶点。本文对α7nAChR的生物学特征及其对围手术期神经认知功能的影响进行综述，以期为临床改善手术患者的围手术期神经认知功能提供新的思路和方法。

α7烟碱型乙酰胆碱受体  /  围手术期，神经认知功能  /  胆碱能抗炎通路  /  中枢神经系统疾病

α7 nicotinic acetylcholine receptor (α7nAChR) is widely expressed in the central nervous system and immune system, and plays a neuro-immunoregulatory role. On the one hand, α7nAChR is involved in the transmission of neurotransmitters, the conduction of excitatory signals and the maintenance of synaptic plasticity, which is of great significance for maintaining the normal and stable neurocognitive function. On the other hand, as an important part of the cholinergic anti-inflammatory pathway, α7nAChR is involved in the regulation of physiological and pathological processes such as inflammatory response, oxidative stress, apoptosis and autophagy in the central system, and plays an immunomodulatory and neuroprotective role, thus being potential target for improving perioperative neurocognitive function. This article reviews the biological characteristics of α7nAChR and its effect on perioperative neurocognitive function, in order to provide ideas and methods for clinical improvement of perioperative neurocognitive function in surgical patients.

α7 nicotinic acetylcholine receptor  /  perioperative period  /  neurocognitive function  /  cholinergic anti-inflammatory pathway  /  central nerve system diseases
司尚坤, 徐迎雪, 张维亮, 季加富, 张栋斌. α7烟碱型乙酰胆碱受体对围手术期神经认知功能的影响研究进展. 解放军医学杂志, 2024 , 49 (3) : 343 -348 . DOI: 10.11855/j.issn.0577-7402.1157.2022.1006
Shang-Kun Si, Ying-Xue Xu, Wei-Liang Zhang, Jia-Fu Ji, Dong-Bin Zhang. Research progress on the effect of α7 nicotinic acetylcholine receptor on perioperative neurocognitive function[J]. Medical Journal of Chinese People’s Liberation Army, 2024 , 49 (3) : 343 -348 . DOI: 10.11855/j.issn.0577-7402.1157.2022.1006
正文
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研究发现，在中枢神经系统(CNS)和免疫系统中广泛分布的α7烟碱型乙酰胆碱受体(α7 nicotinic acetylcholine receptor，α7nAChR)发挥着神经-免疫调节作用[1]。α7nAChR可在神经系统中介导神经递质释放、突触兴奋性传递及细胞间信号转导[2]，参与神经元的形成和突触可塑性维持等生理过程，与维持意识清醒、学习、记忆、专注等密切相关。此外，α7nAChR作为胆碱能抗炎通路(cholinergic anti-inflammatory pathway，CAP)的重要组成部分，可通过胆碱能神经元、神经胶质细胞和多种免疫细胞，抑制过强的炎症反应和氧化应激并维持免疫稳态，还参与自噬、凋亡等下游事件，发挥神经保护作用[1]。围手术期神经认知功能障碍(perioperative neurocognitive disorders，PND)是指围手术期内多个认知领域能力的下降和衰退，包括术前认知功能障碍、术后谵妄(postoperative delirium，POD)、术后认知功能障碍(postoperative cognitive dysfunction，POCD)等[3-4]。目前研究认为，神经炎症反应紊乱和神经元损伤是PND的主要特征，然而PND的具体病理机制尚未完全明确，也缺乏特异的生物标志物[5]。近年来，α7nAChR在炎症反应与免疫调节、神经保护、认知功能改善相关的研究中成为热门靶点，其功能障碍被认为与阿尔茨海默病(Alzheimer disease，AD)、精神分裂症等神经系统疾病有关；α7nAChR激动剂和正向变构调节剂(positive allosteric modulator，PAMs)被广泛报道应用于改善CNS疾病相关的认知障碍，且显示出良好效果[6]。本文对α7nAChR的生物学特征及其对围手术期神经认知功能的影响进行综述，以期为临床预防、诊疗PND提供思路和方法。
1 α7nAChR的生物学特征
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α7nAChR属于配体门控离子通道，是以乙酰胆碱(acetylcholine，Ach)和胆碱作为内源性配体的同源性受体亚型[2]。α7nAChR在中枢海马、皮质和皮质下边缘等区域均有表达，其中在海马组织中含量最高。除神经元外，α7nAChR在神经胶质细胞(如星形胶质细胞和小胶质细胞等)以及多种免疫细胞(如巨噬细胞、树突细胞和T/B淋巴细胞等)中也有表达[7]。人染色体15q14上的烟碱乙酰胆碱受体基因(CHRNA7)编码α7nAChR，而CHRNA7定位/拷贝数错误或功能缺陷与精神分裂症、癫痫、AD等神经疾病相关[2]。
在信号转导方面，α7nAChR参与介导大脑皮层、海马和伏隔核中一系列神经递质(如谷氨酸、多巴胺、去甲肾上腺素、γ-氨基丁酸等)的释放与兴奋性传递。此外，α7nAChR可作为多种细胞过程的次级信使，介导细胞内信号级联和相关下游事件，并参与调节突触的可塑性[7]。由此可见，α7nAChR与学习、记忆等认知行为密切相关。在炎症反应免疫调节与神经保护方面，中枢神经胶质细胞和多种免疫细胞上的α7nAChR作为CAP的重要组成部分，可通过介导PI3K/Akt、核因子-κB(NF-κB)、JAK2/STAT3和Nrf2/HO-1等信号通路调节炎性介质、炎性细胞因子的释放，发挥抗炎、抗氧化应激等作用[8]。此外，α7nAChR还参与调节神经系统中单核/小胶质等细胞的凋亡与自噬[9]，并促进原代皮质神经元突起的生长，提高神经细胞再生活性[10]，从而发挥神经保护作用。
2 α7nAChR与PND的关系
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PND的病理机制尚未明确。目前认为，高龄是PND的独立危险因素，而患者本身的病理生理状态以及麻醉与手术创伤引起的应激紊乱、炎性损伤是PND的重要因素[5]。胆碱能神经系统是CNS的重要组成部分，α7nAChR参与介导神经递质释放、神经元兴奋性传递，还可调节突触后的可塑性水平，对于正常的神经活动尤其是认知功能具有重要意义。
α7nAChR在CNS胆碱能神经元、中枢神经胶质细胞和外周免疫细胞中通过CAP调节炎症反应、氧化应激、细胞凋亡和自噬，对于多种CNS损伤引起的PND可能起到炎症反应免疫调节与神经保护作用。
根据发生时间点PND可分为以下4种[3]。(1)术前认知功能受损：术前即存在的、可以测量的、客观的认知功能受损。(2)术后谵妄(POD)：发生在术后1周内或者出院前，符合精神障碍诊断与统计手册(DSM-5)对谵妄的诊断标准。(3)延迟的神经认知恢复：术后30 d内存在的认知功能减退。(4)术后神经认知障碍：术后30 d至术后12个月存在的认知功能减退。根据现有研究结果，暂时将“延迟的神经认知恢复”和“术后神经认知障碍”归为POCD的范畴以便探讨。以下主要从术前认知功能受损、术后认知功能受损(POD、POCD)两个方面阐述α7nAChR在PND中的作用。
3 α7nAChR在术前认知功能受损中的作用
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大量患者在麻醉手术前即存在临床上或临床前期的认知功能受损，且研究逐步表明术前认知功能损害与术后认知功能减退密切相关[11]，故改善患者术前认知功能对于防治术后认知功能受损具有重要的临床意义。
术前重度认知功能受损临床上可归为神经内科CNS疾病的范畴，如AD、抑郁症、精神分裂症等。研究显示，α7nAChR基因敲除小鼠年龄依赖性AD样病理改变显著增多，提示α7nAChR功能障碍可能先于AD病理改变[12]。研究发现，激活α7nAChR可通过CaM-CaMKII-CREB[13]、Nrf2/HO-1[14]等信号通路调节氧化应激，抑制γ-分泌酶活性，促进海马内β-淀粉样蛋白(amyloid β-protein，Aβ)结合内化，通过诱导小胶质细胞吞噬以及细胞自噬减轻Aβ沉积导致的细胞凋亡和神经损伤，还能维持突触可塑性水平，从而改善AD模型小鼠的认知能力[15]。抑郁症相关研究发现，使用激动剂或PAMs激活α7nAChR可通过作用于PI3K/Akt和ERK/CREB等通路改善大鼠抑郁样行为[16]，提示α7nAChR在抑郁症的发生发展中发挥重要作用。胆碱能与多巴胺能系统之间失衡是精神分裂症的病理生理学假说之一，α7nAChR功能障碍与精神分裂症感觉运动缺陷相关[17]。Unal等[18]研究发现，α7nAChR激动剂和PAMs可以改善MK-801模型大鼠精神分裂症样行为缺陷，其机制可能与调节PDE-4/cAMP、Akt、GSK-3β等通路有关。
总之，α7nAChR与术前认知功能受损密切相关，α7nAChR激动剂或PAMs是改善术前认知功能和预防术后认知功能损害的潜在治疗手段。然而以上研究多基于动物模型，仍需更多的临床试验提供更有说服力的证据支持。此外，对于未满足临床或临床前期神经系统疾病诊断的轻度认知受损与紊乱，有待进一步研究探索α7nAChR是否对其具有改善作用。
4 α7nAChR在术后认知功能受损中的作用
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POD是麻醉手术后早期常见的急性、波动性认知紊乱并发症，主要表现为思维混乱、意识/记忆水平障碍、专注力下降，同时常产生幻错觉、焦虑等精神障碍[19]。POCD是全身麻醉手术后常见的远期CNS并发症，主要表现为思维、定向、记忆和专注力障碍及精神、人格改变或社会活动能力降低[20]。POCD可由POD发展而来，其病情会随病程不断加重，若不及时诊治可造成严重的记忆损害、痴呆和性格行为改变等AD前期表现。及时预防、诊断及干预POD和POCD对于改善患者术后认知和生活质量具有重要的现实意义。
4.1 术后认知功能受损病理机制
POD与POCD的病理机制相似，不同之处在于POD是术后急性认知受损，其病因多为术后短时间内机体神经-体液-内分泌系统的紊乱与失衡导致的急性神经认知功能下降，若术后慢性炎症反应和病理损害长时间仍未逆转或缓解则可能迁延发展成为POCD。现有研究认为，除高龄这一独立危险因素外，CNS炎症反应紊乱、胆碱能系统功能障碍、细胞凋亡、氧化应激损伤、睡眠生理节律紊乱等因素是术后认知功能损害的重要发病机制[21]。目前，有关α7nAChR在POD和POCD中的研究主要集中于神经炎症反应紊乱和胆碱能系统功能障碍。
4.1.1 神经炎症反应紊乱
麻醉、机械通气与手术等操作致使应激反应失调、大量炎性趋化因子释放，与缺血、缺氧及疼痛等因素相叠加，可破坏血脑屏障的超微结构并激活神经胶质细胞，造成CNS级联炎症反应紊乱、突触可塑性破坏及神经元损伤，是POD和POCD发生的重要机制[21]。研究发现，α7nAChR下调以及下游PI3K/Akt/GSK-3β通路活性降低可增高小胶质细胞和星形胶质细胞的活化水平，引起神经炎症反应[22]。此外，手术和麻醉可抑制神经和免疫细胞上的α7nAChR，使mtROS/NLRP3/IL-1β信号通路过度表达，从而导致炎症反应紊乱与损伤，同时也可能是术后早期认知功能受损的潜在干预靶点[23]。有研究发现，挥发性麻醉剂可促使N-甲基-D-天冬氨酸受体(N-methyl-D-aspartic acid receptor，NMDAR)内化并产生麻醉神经毒性，引起树突棘的改变及认知障碍，而NMDAR在海马中的转运与α7nAChR密切相关[24]。由此可见，麻醉、手术等因素与α7nAChR功能异常所致神经炎症反应紊乱可能是术后认知功能下降的重要发病机制。
4.1.2 胆碱能系统障碍
胆碱能神经系统学说认为，抗胆碱能活性增强导致α7nAChR介导的CAP失调可能是神经认知功能受损的分子机制[1]。Lin等[25]发现，脑脊液中胆碱能生物标志物与老年患者POD的发生相关，提示老年患者中枢胆碱能退化可导致认知储备下降。同时临床使用抗胆碱能药物也可能导致POD和POCD风险增高，Yilmaz等[26]发现术中输注多巴胺是POD发生的独立危险因素，其机制可能与纹状体中多巴胺会对ACh起到拮抗作用有关。麻醉时应用非去极化神经肌肉阻滞剂对神经元烟碱型乙酰胆碱受体(nicotinic acetylcholine receptors，nAChRs)具有浓度依赖性的抑制作用，使用异氟醚等吸入麻醉药物可造成基底前胆碱能神经元数量减少、Ach转移酶(choline acetyltransferase，ChAT)活性降低，减少中枢胆碱释放、抑制突触后nAChRs，导致海马和杏仁核内α7nAChR功能紊乱，最终损害术后学习及记忆功能[27]。同时，手术应激状态可产生具有神经毒性的Aβ并增加乙酰胆碱酯酶(acetylcholinesterase，AchE)活性，引起包括α7nAChR在内的胆碱能功能障碍，影响患者认知功能[28]。此外，有荟萃分析发现，血清抗胆碱能活性可以反映CNS的抗胆碱负荷，对谵妄的发生有一定预示作用，具有辅助诊断谵妄的潜在价值[29]。以上结果表明，包含α7nAChR在内的胆碱能功能障碍及CAP失调可能是术后认知功能下降的重要病理机制。
4.2 术后认知功能受损的作用
4.2.1 调节神经炎症反应紊乱
Terrando等[30]较早提出激活α7nAChR可能通过内源性抗炎途径抑制肿瘤坏死因子-α(tumor necrosis factor-α，TNF-α)诱导的NF-κB激活，减少中枢免疫细胞向海马的迁移，改善麻醉与手术对认知功能的损害；后续研究进一步发现，使用α7nAChR激动剂对胫骨骨折模型小鼠具有神经保护作用，可显著改善神经炎症反应和海马依赖性记忆功能障碍，其机制可能与调节NF-κB和氧化应激还原型辅酶Ⅱ信号有关[31]。现有研究认为，α7nAChR激活后主要作用于神经胶质细胞和巨噬细胞等，通过JAK2/STAT3、NF-κB、TNF-α转化酶等通路减少高迁移率族蛋白B1(high mobility group protein 1，HMGB1)等促炎因子的表达与释放，使抗炎细胞因子白细胞介素-10(interleukin-10，IL-10)水平升高，并抑制NLRP3炎性小体的激活[32]，降低CD4+IL-17+细胞的数量，抑制TH17免疫应答[33]，产生抗炎作用并改善神经元凋亡，降低POD及POCD发生率。有研究发现，应用α7nAChR激动剂GTS-21能抑制海马炎性损伤，缓解异氟醚导致的术后认知损害[27]。Zhu等[34]发现，右美托咪定预处理可通过α7nAChR依赖性机制，减轻海马小胶质细胞和星形胶质细胞的过度表达，抑制NF-κB活性，降低TNF-α和IL-1β水平，减轻大鼠胫骨骨折引起的神经炎症反应和POCD。还有研究发现，5-羟色胺-3(5-HT3)受体拮抗剂托烷司琼可激活α7nAChR，通过调节p38MAPK-CREB通路，降低IL-6、IL-1β和TNF-α等炎性介质水平，减轻神经炎症反应[35]，从而降低成人非心脏POD的可能性[36]。此外，中医针刺刺激百会穴、内关穴、足三里穴可上调α7nAChR的表达，抑制海马CA1区小胶质细胞、肥大细胞活性，通过调节HMGB1-NF-κB、JAK2/STAT3等通路，降低海马炎性细胞因子水平，抑制神经元损伤，改善胫骨骨折手术模型大鼠POCD[37]。
4.2.2 改善胆碱能系统障碍
通过使用胆碱能活性药物或刺激迷走神经等措施可提高胆碱能通路活性，促进Ach释放、上调ChAT水平，激活外周和大脑免疫细胞上的α7nAChR并通过CAP抑制海马区小胶质细胞的活化，减少炎性介质、促炎性细胞因子的释放，减轻海马区炎症反应，可能对于改善麻醉与手术所造成的认知功能障碍有所裨益[38]。Huang等[39]使用nAChRs激动剂伐伦克兰提高包括α7nAChR在内的胆碱能系统活性，可通过JAK2/STAT3通路减轻Tau蛋白磷酸化和DNA损伤，改善老年雄性小鼠麻醉剖腹手术后的神经炎症反应与神经元凋亡，减轻术后认知功能损伤。应用AChE抑制剂提高胆碱能活性可减轻髋部骨折手术老年患者的氧化应激反应，降低POD的发生率[40]，AChE抑制剂如多奈哌齐、毒扁豆碱、新斯的明等也被报道用于预防麻醉手术造成的POCD[41]。研究发现，围手术期应用右美托咪定可减轻交感神经对迷走神经的抑制，促进Ach的释放，提高胆碱能神经系统的兴奋性，并通过调节脑内AchE及海马组织ChAT水平，激活α7nAChR和CAP，通过PI3K/Akt、TLR4等通路，降低海马区IL-1β、IL-6等炎性因子的表达，发挥抗炎与神经保护作用，降低POD的发生风险[42]。此外，有研究发现，耳廓迷走神经刺激术可增加胆碱能活性，促进迷走神经远端释放ACh，并上调海马内神经胶质细胞与免疫细胞上α7nAChR的表达，缓解海马神经元凋亡，并通过CAP降低TNF-α、IL-1β和NF-κB水平，缓解剖腹探查老年模型大鼠的POCD症状[43]。刘冬等[44]发现，κ阿片受体激动剂可激活CAP，上调α7nAChR的表达，改善体外循环后大鼠的认知功能。郭雨微等[45]发现，每月饮用绿茶量多、脑脊液中高浓度咖啡因和茶多酚可降低老年患者POD的发生，其机制可能与茶叶中所含的茶多酚和咖啡因可增强包括α7nAChR在内的胆碱能神经活性与神经传递有关。
综上所述，通过使用α7nAChR的激动剂、PAMs或拟胆碱能药物等措施激活α7nAChR通路，提高胆碱能神经活性，调节中枢免疫紊乱与炎症反应损伤，可以作为防治术后认知功能受损的潜在手段，且具有巨大潜在价值。
5 总结与展望
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大量研究证实了α7nAChR与PND之间的相关性。使用α7nAChR选择性激动剂、PAMs等靶向药物如GTS-21、PNU-282987和PNU-120596及拟胆碱能活性药物激活神经胶质细胞和免疫细胞上的α7nAChR，增强胆碱能通路的活性，可通过CAP抑制炎症反应，并能调节氧化应激、细胞凋亡和自噬，起到神经保护作用，对改善PND具有巨大的临床潜在价值。此外，α7nAChR及血清抗胆碱活性等胆碱能生物标志物可能对PND发挥一定的辅助诊断作用。然而，关于α7nAChR的生理功能、下游调控靶点及传导通路尚未完全明确并存在争议，目前有关α7nAChR在PND中作用的研究多为动物实验，尚需要更多的临床验证。随着对α7nAChR及其下游通路研究的不断深入，可从炎症反应紊乱、胆碱能系统障碍等方面进一步揭示PND的发病机制，并为改善目前PND对症治疗的现状提供思路和方法。
基金
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  • 山东省自然科学基金面上项目(ZR2021MH168)
  • 山东省自然科学基金面上项目(ZR2020MH391)
文献
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2024年第49卷第3期
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doi: 10.11855/j.issn.0577-7402.1157.2022.1006
  • 接收时间：2022-05-20
  • 首发时间：2025-11-23
  • 出版时间：2024-03-28
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  • 收稿日期：2022-05-20
  • 录用日期：2022-09-18
基金
Natural Science Foundation of Shandong Province(ZR2021MH168)
山东省自然科学基金面上项目(ZR2021MH168)
Natural Science Foundation of Shandong Province(ZR2020MH391)
山东省自然科学基金面上项目(ZR2020MH391)
作者信息
    1山东中医药大学中医学院，山东济南 250014
    2山东中医药大学附属医院麻醉科，山东济南 250014

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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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