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Article(id=1200026649170379600, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1200026645001241395, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.1125.2022.0908, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1652716800000, receivedDateStr=2022-05-17, revisedDate=null, revisedDateStr=null, acceptedDate=1657209600000, acceptedDateStr=2022-07-08, onlineDate=1764038248579, onlineDateStr=2025-11-25, pubDate=1693152000000, pubDateStr=2023-08-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1764038248579, onlineIssueDateStr=2025-11-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1764038248579, creator=13701087609, updateTime=1764038248579, updator=13701087609, issue=Issue{id=1200026645001241395, tenantId=1146029695717560320, journalId=1189873630562394117, year='2023', volume='48', issue='8', pageStart='871', pageEnd='992', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1764038247584, creator=13701087609, updateTime=1764038741950, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1200028718564474883, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1200026645001241395, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1200028718564474884, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1200026645001241395, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=972, endPage=977, ext={EN=ArticleExt(id=1200026649770165076, articleId=1200026649170379600, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Research progress on the relationship between high mobility group box 1 and sepsis-associated encephalopathy, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Sepsis-associated encephalopathy (SAE) is a complex disease with high mortality, an urgent clinical problem to be solved. The mechanism of SAE has not been fully elucidated and there is no effective treatment. Recent study found that high mobility group box 1 (HMGB1) is a late-stage pro-inflammatory mediator with the effect of activating inflammation, besides, HMGB1 plays important role in tissue repair, as well as in sepsis-induced brain injury. Therefore, In-depth research on the relationship between HMGB1 and SAE is expected to provide a new direction for the diagnosis and treatment of SAE. This review focuses on current status of SAE, HMGB1 and the four aspects of HMGB1, including impairment of blood-brain barrier, dysregulation of immune response, oxidative stress and neuronal apoptosis that involved in brain function impairment and SAE.

, correspAuthors=Xi-Jing Zhang, authorNote=null, correspAuthorsNote=
E-mail:
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脓毒症相关脑病(SAE)病情复杂且病死率高，是亟待解决的临床问题；目前其发病机制尚未完全阐明，尚无有效治疗方法。脑内高迁移率族蛋白B1(HMGB1)是一种促炎介质，具有激活炎症及组织修复作用，在脓毒症诱导的脑损伤中发挥潜在作用。因此，深入研究HMGB1与SAE之间的关系，有望为SAE的诊断及治疗提供新方向。本文就SAE的现状以及HMGB1通过介导免疫炎症、氧化应激、神经细胞凋亡和血脑屏障损伤而导致SAE的机制研究进展进行综述。

, correspAuthors=张西京, authorNote=null, correspAuthorsNote=
张西京，E-mail：
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原娇娇，医学硕士，主要从事脓毒症等方面的研究

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原娇娇，医学硕士，主要从事脓毒症等方面的研究

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原娇娇，医学硕士，主要从事脓毒症等方面的研究

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高迁移率族蛋白B1与脓毒症相关脑病关系的研究进展
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原娇娇 , 方宗平 , 张西京 *
解放军医学杂志 | 综述 2023,48(8): 972-977
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解放军医学杂志 | 综述 2023, 48(8): 972-977
高迁移率族蛋白B1与脓毒症相关脑病关系的研究进展
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原娇娇, 方宗平, 张西京*
作者信息
  • 空军军医大学西京医院重症医学科，陕西西安 710000

    • 原娇娇，医学硕士，主要从事脓毒症等方面的研究

通讯作者:

张西京，E-mail：
Research progress on the relationship between high mobility group box 1 and sepsis-associated encephalopathy
Jiao-Jiao Yuan, Zong-Ping Fang, Xi-Jing Zhang*
Affiliations
  • Department of Critical Care Medicine, Xijing Hospital, Air Force Military Medical University, Xi'an, Shaanxi 710000, China
出版时间: 2023-08-28 doi: 10.11855/j.issn.0577-7402.1125.2022.0908
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摘要
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脓毒症相关脑病(SAE)病情复杂且病死率高，是亟待解决的临床问题；目前其发病机制尚未完全阐明，尚无有效治疗方法。脑内高迁移率族蛋白B1(HMGB1)是一种促炎介质，具有激活炎症及组织修复作用，在脓毒症诱导的脑损伤中发挥潜在作用。因此，深入研究HMGB1与SAE之间的关系，有望为SAE的诊断及治疗提供新方向。本文就SAE的现状以及HMGB1通过介导免疫炎症、氧化应激、神经细胞凋亡和血脑屏障损伤而导致SAE的机制研究进展进行综述。

脓毒症  /  脓毒症相关脑病  /  高迁移率族蛋白B1

Sepsis-associated encephalopathy (SAE) is a complex disease with high mortality, an urgent clinical problem to be solved. The mechanism of SAE has not been fully elucidated and there is no effective treatment. Recent study found that high mobility group box 1 (HMGB1) is a late-stage pro-inflammatory mediator with the effect of activating inflammation, besides, HMGB1 plays important role in tissue repair, as well as in sepsis-induced brain injury. Therefore, In-depth research on the relationship between HMGB1 and SAE is expected to provide a new direction for the diagnosis and treatment of SAE. This review focuses on current status of SAE, HMGB1 and the four aspects of HMGB1, including impairment of blood-brain barrier, dysregulation of immune response, oxidative stress and neuronal apoptosis that involved in brain function impairment and SAE.

sepsis  /  sepsis-associated encephalopathy  /  high mobility group box 1
原娇娇, 方宗平, 张西京. 高迁移率族蛋白B1与脓毒症相关脑病关系的研究进展. 解放军医学杂志, 2023 , 48 (8) : 972 -977 . DOI: 10.11855/j.issn.0577-7402.1125.2022.0908
Jiao-Jiao Yuan, Zong-Ping Fang, Xi-Jing Zhang. Research progress on the relationship between high mobility group box 1 and sepsis-associated encephalopathy[J]. Medical Journal of Chinese People’s Liberation Army, 2023 , 48 (8) : 972 -977 . DOI: 10.11855/j.issn.0577-7402.1125.2022.0908
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脓毒症病死率高、预后差，是目前全世界面临的医学难题之一[1-2]。在脓毒症的病理进程中，大脑起着重要作用，因其既可调控免疫反应，又是病理过程的靶器官，因此常成为首先受累的器官之一[3]；大脑受累后主要表现为脓毒症相关脑病(sepsis-associated encephalopathy，SAE0)，其定义为在大脑无直接感染证据的前提下，由脓毒症引起的全身炎症反应所致的弥漫性或多灶性脑功能障碍。有研究表明，脑内高迁移率族蛋白B1(high mobility group box 1，HMGB1)在SAE发生、发展中起重要作用[4-5]，深入研究HMGB1与SAE之间的关系，有望为SAE的诊断及治疗提供新方向。本文就SAE的现状以及HMGB1通过介导免疫炎症、氧化应激、神经细胞凋亡和血脑屏障损伤而导致SAE的机制研究进展进行综述。
1 SAE现状
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约50%的脓毒症患者在重症监护病房(ICU)发生SAE，出现SAE的脓毒症患者病死率明显增高[4-5]。SAE诊断复杂，需要排除脓毒症患者的其他脑病原因(如代谢变化、药物中毒、脑结构病变、脑血管事件、脑炎、脑膜炎、非惊厥性癫痫持续状态)后才能确诊[6]。而早期意识水平改变是SAE的特征表现，症状范围从行为改变、焦虑、谵妄到昏迷，随后可能导致长期认知障碍[7]。近年来，有关SAE的发病机制研究主要集中于神经炎症、线粒体功能障碍及血脑屏障损伤方面[8]。到目前为止，SAE的确切发病机制、统一命名方法、诊断标准仍然不清楚[9]，而且缺乏特异性的诊断指标以及有效的治疗方法。
有尸检发现，SAE对中枢神经系统造成的损害是永久性的[10]。因此，早期确定SAE的独立危险因素对评估预后及后期治疗至关重要。SAE的确定危险因素包括高龄、高血压、胃肠道感染、肠球菌感染、血小板计数下降、急性肾衰竭、低血糖、高糖血症、高碳酸血症及高钠血症[11]。既往存在认知障碍、精神状态改变、神经系统疾病、长期使用精神活性药物、酗酒、慢性肝病、免疫抑制的患者[12]及金黄色葡萄球菌、不动杆菌和铜绿假单胞菌引起的胆道感染患者[13]，SAE发生率明显增高。
目前实验室检查尚未确定诊断SAE的特异性生物标志物[14]。但有研究表明序贯器官衰竭估计评分(sequential orange failure assessment，SOFA)及急性生理与慢性健康评分Ⅱ(acute physiology and chronic health evaluation Ⅱ，APACHE Ⅱ)与SAE的28 d病死率独立相关[11，15]。而腹腔内高压[16]、神经元特异性烯醇化酶(neuron-specific enolase，NSE)、S100β蛋白及血浆C型利钠肽的氨基末端前肽(N-terminal propeptide of CNP，NT-proCNP)峰值浓度升高与SAE的发生明显相关(其中S100β蛋白水平测定优于NSE水平[13]，而血浆NT-proCNP水平测定可能优于NSE及S100β水平[17])。另外，脑脊液中髓系细胞可溶性触发受体2(soluble triggering receptor expressed on myeloid cells 2，sTREM2)及神经纤维轻链(neurofilament light chain，NFL)水平升高可作为SAE患者认知能力下降的预后指标[18-19]。通过气相色谱-质谱方法检测的血浆代谢物4-羟基苯乙酸(4-hydroxyphenylacetic acid，4-HPA)与意识障碍的严重程度明显相关[20]。
2 HMGB1
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有研究发现，HMGB1与格拉斯哥昏迷量表(GCS)评分及C反应蛋白水平高度相关，且HMGB1的预测价值与GCS评分相似，因而推测脑组织中HMGB1浓度可能是预测SAE的一种新的生物标志物[21]。但目前有关SAE的发病机制研究主要集中于神经炎症、线粒体功能障碍及血脑屏障损伤方面[8]。早期认为HMGB1是细胞核中的结构蛋白，具有稳定DNA结构并调节转录的作用[22]，而目前发现它还是一种促炎介质，具有激活炎症及修复组织的作用[23]。根据其分子位置(在细胞核中、细胞质中或细胞外)、结合受体及氧化还原状态的不同，可在不同阶段发挥不同的临床作用[24]。有研究发现，在炎症、创伤、应激后可由坏死细胞被动释放HMGB1，也可由活化的炎性细胞主动分泌释放HMGB1[21，23]，接着HMGB1发生易位(在30 min~1 d内转移到损伤区细胞的细胞质中，在2~20 d内转移到吞噬小胶质细胞的细胞质中)，然后以旁分泌及自分泌的方式触发促炎介质的表达。在脓毒症诱导脑损伤的过程中，脑组织中可检测到HMGB1，而应用HMGB1单克隆抗体(中和型抗HMGB1单克隆抗体)可抑制HMGB1易位及炎症分子表达，保护血脑屏障完整性并改善运动功能[25]。
3 HMGB1与SAE
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有研究显示在脓毒症诱导的脑损伤中HMGB1发挥了潜在作用[23]。HMGB1在神经炎症、线粒体功能障碍及血脑屏障损伤方面扮演了重要角色，其中在神经炎症及线粒体功能障碍方面主要表现为神经元损伤，而在血脑屏障损伤方面则表现为内皮细胞损伤。
3.1 HMGB1介导神经炎症而影响SAE的发生
Ren等[26-27]为研究HMGB1对脓毒症大鼠脑损伤的影响，在大鼠脑室注射HMGB1特异性拮抗剂BoxA，结果发现，与脓毒症组大鼠相比，10 μg的BoxA脑室给药可明显减轻多脏器功能损伤[如降低血清谷丙转氨酶(alanine amino transferase，ALT)、谷草转氨酶(aspartate amino transferase，AST)、甘氨胆酸(cholylglycine，CG)、肌酸激酶(creatine kinase，CK)、肌酸激酶同工酶(creatine kinase isoenzymes，CK-MB)、血尿素氮(blood urea nitrogen，BUN)及肌酐(creatinine，Cr)水平，以及降低髓过氧化物酶(myeloperoxidase，MPO)活性及肺的湿/干重(W/D)比值等]，逆转脓毒症对CD4+ T细胞增殖的抑制作用，且明显提高脓毒症大鼠的存活率(脓毒症+10 μg BoxA组 vs. 脓毒症组：62% vs. 30%，P<0.05，n=26)，降低S100β及NSE水平(P<0.05)；免疫荧光检测结果显示，与假手术组比较，脓毒症组各脑区HMGB1蛋白水平均明显升高，抑制脑HMGB1后，可明显改善记忆、学习及运动功能障碍，还可减少细胞凋亡(脓毒症组TUNEL染色阳性细胞明显增多)。上述研究不仅提示HMGB1在脑组织中表达，还表明抑制HMGB1对脓毒症相关脑损伤具有较强的保护作用。因此，HMGB1可能是预防或改善SAE的早期拮抗靶点，而中枢HMGB1可能是SAE的潜在治疗靶点，通过脑室内给予HMGB1特异性拮抗剂BoxA可能改善SAE的预后。
SAE早期表现类似于炎症反应综合征相关的脑病，其发病原因是炎性介质(细胞因子)的产生[28]。神经炎症的特征是产生促炎性细胞因子[如白细胞介素(IL)-1β、肿瘤坏死因子-α(TNF-α)、IL-6、HMGB1]，过度激活小胶质细胞及炎性细胞浸润[29]。
3.1.1 产生促炎性细胞因子HMGB1
有研究表明，脂多糖及TNF-α可通过不同途径刺激单核细胞/巨噬细胞分泌HMGB1。HMGB1的分泌需要3个步骤：一是从细胞核易位至细胞质，二是从细胞质中转位到细胞器，三是结合Toll样受体(Toll-like receptor，TLRs)后8~12 h主动分泌到细胞外环境中，并发挥细胞外作用——HMGB1的累积增加(自损伤后16 h内)可以放大细胞因子级联反应，刺激炎症反应，介导炎症反应的损伤[30]。当发生神经性炎症及缺血性损伤时，会导致大脑功能障碍，大脑功能紊乱后可破坏免疫稳态，进一步造成顽固性免疫功能障碍及神经内分泌免疫网络(如胆碱能抗炎通路、下丘脑-垂体-肾上腺轴、交感神经系统)的破坏，这些神经调节机制的功能障碍(包括中性粒细胞、巨噬细胞/单核细胞、树突状细胞、T淋巴细胞在内的外周免疫细胞计数减少及异常反应)会进一步危害系统免疫反应，最终导致脑损伤与免疫反应之间的恶性循环[31]。脓毒症后免疫应答的内稳态对维持中枢神经系统功能的完整性具有重要意义，因此，阻断SAE与外周免疫失调之间的恶性循环可能是治疗SAE的有效策略，在这个过程中，HMGB1发挥了介导免疫炎症的重要作用。
3.1.2 过度激活小胶质细胞
尸检研究显示，脓毒症患者脑灰质及白质的小胶质细胞均被大量激活，因此小胶质细胞可能是神经炎症反应的重要靶细胞[32]。核苷酸结合寡聚化结构域样受体家族含热蛋白结构域蛋白3(NOD-like receptor family pyrin domain containing protein 3，NLRP3)是一种炎性小体传感器蛋白，它的激活导致与凋亡相关的斑点样蛋白(apoptosis-associated speck-like protein containing a CARD，ASC)及含半胱氨酸的天冬氨酸蛋白水解酶(caspase)-1在内的低聚蛋白复合物——炎性小体的形成[33]。而Gustin等[34]首次证实小胶质细胞是神经炎症反应的靶细胞，小胶质细胞、星形胶质细胞中均有HMGB1 mRNA及蛋白表达。但在星形胶质细胞中，尽管caspase-1为低水平表达，但几乎没有检测到NLRP3及ASC转录物的表达，且无法观察到星形胶质细胞分泌IL-1β，提示其缺乏功能性NLRP3炎性小体，仅在小鼠大脑中的小胶质细胞室发现功能性NLRP3炎性小体，且小胶质细胞对不同的经典炎性小体激活剂均可反应性分泌IL-1β。
3.1.3 炎性细胞浸润
动物实验研究证实，HMGB1激活小胶质细胞后可导致炎性细胞浸润，在SAE小鼠中抑制HMGB1可下调炎性小体NLRP3的表达，减轻神经炎症及认知障碍[35]。此外，Kim等[36]还发现，HMGB1通过与多种受体或配体结合，既具有促炎作用又具有抗炎作用，HMGB1在炎症发生时可能触发促炎巨噬细胞，但随着补体1q(C1q)水平的升高并与白细胞免疫相关受体(leukocyte-associated Ig-like receptor，LAIR-1)结合，单核细胞可能向抗炎巨噬细胞倾斜。促炎与抗炎反应的平衡主要取决于C1q水平，HMGB1与C1q结合是激活补体系统的经典途径，经典补体途径的慢性激活，无论是通过HMGB1的累积，还是通过其与内源性分子如β淀粉样蛋白(amyloid β-protein，Aβ)的协同作用，都可能触发无菌性炎症。因此，通过补体激活HMGB1介导的无菌性炎症是治疗慢性炎症的一个新思路。
线粒体是氧化应激及能量代谢的调节中心，氧化应激后最终可导致细胞凋亡及坏死[37]，因而在此将线粒体功能障碍分为氧化应激及神经细胞凋亡两方面进行叙述。
3.2 HMGB1介导氧化应激而影响SAE的发生
有研究证实，在脓毒症动物的不同脑区均出现早期线粒体功能障碍，导致ATP及氧/氮活性物质生成减少[7]。氧化应激是SAE最重要的触发因素之一，在脓毒症期间，会产生大量机体无法消除的活性氧(reactive oxygen species，ROS)，ROS可诱导脂质过氧化，而丙二醛(MDA)是脂质过氧化的直接产物，因此被用来评估脂质过氧化的严重程度；ROS可损伤细胞、线粒体膜，最终导致细胞凋亡及坏死，在抗氧化系统中，超氧化物歧化酶(SOD)及过氧化氢酶(CAT)是ROS的清除剂，它们的活性水平代表了ROS的清除状态。SAE发生时，SOD、CAT活性水平明显降低，而MDA水平明显升高[29]。HMGB1在调节细胞内外应激的细胞反应中发挥着重要作用，尽管HMGB1激活后调控个体信号转导的机制仍在研究中，但氧化应激似乎是导致HMGB1易位、释放及炎性细胞死亡的主要调节因素[38]。还有研究表明，HMGB1可以通过激活丝氨酸/苏氨酸蛋白激酶3(receptor-interacting serine/threonine-protein kinase 3，RIPK3)微调线粒体体积或数量，从而调节线粒体功能[39]。HMGB1是氧化应激下的传感器，机体通过协调应激反应(如自噬)来应对氧化损伤，以防止进一步损伤[40]。Li等[41]发现，HMGB1过表达可降低大鼠脑组织小胶质细胞中SOD、IL-4及IL-10水平，提高IL-1β、TNF-α及MDA水平，从而增强氧化应激，促进炎性因子分泌及加重脑损伤，进一步诱导脑组织凋亡；另外，miR-103a-3p可直接结合到HMGB1的3'非编码区域并调控基因表达(如抑制miRNA翻译或诱导miRNA切割)，过表达miR-103a-3p会抑制HMGB1的表达，从而产生与上述作用相反的效果，且miR-103a-3p通过靶向HMGB1可减轻脂多糖诱导的小胶质细胞氧化应激及凋亡，因此推测HMGB1是miR-103a-3p的作用靶点，靶向HMGB1可减轻氧化应激反应。由于HMGB1在SAE中发挥介导氧化应激的传感器作用，因此阻断或抑制HMGB1的表达可能是治疗SAE的一种新策略。
3.3 HMGB1诱导神经细胞凋亡而影响SAE的发生
HMGB1在脓毒症反应中诱导脑细胞凋亡的具体机制主要有：脓毒症脑损伤后，HMGB1被活跃的免疫细胞(包括巨噬细胞、单核细胞及中性粒细胞)释放并从胞核易位到胞质，释放后与晚期糖基化终末产物受体(receptor for advanced glycation endproduct，RAGE)结合，激活核因子(NF)-κB信号通路，参与炎症、凋亡、增殖及自噬的调控[42]。SAE可引起线粒体功能障碍，导致ATP耗竭及细胞凋亡，TNF-α也可导致细胞凋亡，这两种凋亡途径都会导致caspase的激活，进而参与细胞凋亡[29]。Caspase是细胞凋亡信号转导的常用途径，在促凋亡因子的作用下，caspase相互激活并启动特异性的caspase级联反应，最终导致细胞发生凋亡[43]。有研究发现，脓毒症小鼠中caspase-3活性明显升高，但阻断脑HMGB1后caspase-3活性明显下降[26]，推测HMGB1损害的脑细胞凋亡可能作用于caspase-3。
在中性粒细胞胞外诱捕网(neutrophil extracellular traps，NETs)形成过程中伴随着中性粒细胞的死亡，这种新型的死亡方式不同于细胞凋亡及细胞坏死，被称为NETosis[44]。Kim等[45]发现，HMGB1在脑实质及外周血中性粒细胞瓜氨酸化组蛋白H3+(citrullinated histone H3+，CitH3，NETosis的标记物)诱导中发挥了重要作用——HMGB1不仅诱导NETosis，而且是NETosis过程中挤压出的细胞内容物的组成部分，挤压出的HMGB1可能作为一种损伤相关分子(danger associated molecular pattern，DAMP)激活中性粒细胞及其他免疫细胞，加剧炎症反应，进一步作用于NETosis介导的神经元死亡；由于与NETs共定位，细胞外HMGB1也由NETosis提供，应用HMGB1 BoxA阻断HMGB1不仅可抑制N-甲基-D-天冬氨酸受体(N-methyl-D-asparticacidreceptor，NMDA)条件培养基诱导的NETosis，还可减少NETosis诱导的神经元死亡。因此，HMGB1介导了神经元细胞死亡与NETosis之间的恶性循环，通过调节HMGB1靶向NETosis，可能为减轻缺血性脑损伤提供一种新的治疗策略。
3.4 HMGB1导致血脑屏障损伤而影响SAE的发生
血脑屏障主要由形成血管壁的内皮细胞及位于内皮细胞层腔壁表面的壁细胞组成，由壁细胞、免疫细胞、胶质细胞及神经细胞相互诱导并维持正常功能。血脑屏障通过限制白细胞从外围向中枢神经系统的浸润，在大脑免疫中发挥重要作用，一旦屏障缺陷会导致脑水肿形成及微血管灌注减少，加剧SAE中的神经元凋亡[46]。在脓毒症死亡患者的脑组织样本中，微血管内皮细胞中紧密连接蛋白闭合蛋白(occludin)、密封蛋白(claudin)-5及紧密连接蛋白-1(zonula occluden-1，ZO-1)明显下调，提示其血脑屏障功能受损[47]。紧密连接的跨膜分子包括occludin、claudin及连接黏附分子(junctional adhesion molecules，JAMs)；occludin是中枢神经屏障的重要组成部分，claudin是紧密连接链的主要成分，而JAMs可调节白细胞外渗及细胞旁通透性，细胞质斑块蛋白ZO-1及ZO-2则直接调控紧密连接链在上皮细胞中的形成及定位[46，48]。有研究表明，脓毒症期间血脑屏障的完整性受到损害，血清中脂多糖诱导的细胞因子及危险信号分子直接破坏血脑屏障，改变了血脑屏障功能，包括吸附后转胞吞作用、免疫细胞转运及其他转运功能，从而促进细胞旁渗漏、重新诱导泡突及胞质渗漏，导致促炎免疫细胞及分子进入中枢神经系统[49]。
TLRs是一类高度保守的蛋白，可激活先天免疫细胞以应对各种内、外源性刺激。据报道，TLR2及TLR4参与了HMGB1的信号转导，其中TLR4可能是激活巨噬细胞并介导细胞因子释放及组织损伤的主要受体，RAGE可能是HMGB1介导巨噬细胞和肿瘤细胞趋化性及细胞因子活性的受体[30]。Evran等[50]发现，HMGB1从坏死细胞释放后会诱导炎症反应，在促进TLR4及RAGE表达的同时，还可降低occludin、claudin-5及ZO-1的表达，后者通过影响血脑屏障中的紧密连接分子而破坏血脑屏障，从而导致脑水肿，并进一步增加细胞凋亡及氧化应激等继发性损伤。Li等[51]发现，HMGB1水平升高与血脑屏障受损及随后的神经炎症相关，黄芩苷(baicalin，BAI)可在海马小胶质细胞中通过SIRT1/HMGB1信号通路抑制HMGB1的释放，并抑制HMGB1的乙酰化及易位，从而减弱小胶质细胞的激活，减轻了神经炎症。
总之，HMGB1蛋白可通过破坏血脑屏障而导致神经炎症，最终造成脑功能障碍，发生SAE，对这一点进行深入研究，可能会找到SAE治疗的新方向。
4 总结与展望
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HMGB1可通过破坏血脑屏障，介导免疫炎症、氧化应激及神经细胞凋亡造成大脑功能受损而发生SAE，在这个过程中HMGB1参与了各个步骤并最终介导SAE的发生，因此，抑制HMGB1的释放、易位可能是治疗SAE的重要途径。这一发现可以为SAE的治疗提供一种新的策略及思路，不仅可早期干预脓毒症诱导的脑损伤，还可通过打破这种恶性循环或通路来逆转免疫紊乱、神经炎症及凋亡的发生，为早期进行SAE预警、明确诊断及改善预后奠定基础。由于上述4种机制的研究大多仅限于动物实验阶段，因此仍需通过临床研究确定HMGB1是否为SAE临床上可行的治疗靶点，从而将动物研究结果转化为临床应用。
基金
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  • 国家自然科学基金(81871603)
  • 国家自然科学基金(82171322)
文献
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2023年第48卷第8期
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doi: 10.11855/j.issn.0577-7402.1125.2022.0908
  • 接收时间：2022-05-17
  • 首发时间：2025-11-25
  • 出版时间：2023-08-28
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  • 收稿日期：2022-05-17
  • 录用日期：2022-07-08
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National Natural Science Foundation of China(81871603)
国家自然科学基金(81871603)
National Natural Science Foundation of China(82171322)
国家自然科学基金(82171322)
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    空军军医大学西京医院重症医学科，陕西西安 710000

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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
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光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
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