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Article(id=1208791318986354747, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208791311621157694, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.2021.11.16, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1611590400000, receivedDateStr=2021-01-26, revisedDate=1619020800000, revisedDateStr=2021-04-22, acceptedDate=null, acceptedDateStr=null, onlineDate=1766127908703, onlineDateStr=2025-12-19, pubDate=1638028800000, pubDateStr=2021-11-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1766127908703, onlineIssueDateStr=2025-12-19, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1766127908703, creator=13701087609, updateTime=1766127908703, updator=13701087609, issue=Issue{id=1208791311621157694, tenantId=1146029695717560320, journalId=1189873630562394117, year='2021', volume='46', issue='11', pageStart='1061', pageEnd='1164', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1766127906946, creator=13701087609, updateTime=1766128932678, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1208795613920104935, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208791311621157694, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1208795613920104936, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208791311621157694, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=1159, endPage=1164, ext={EN=ArticleExt(id=1208791320466944083, articleId=1208791318986354747, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Mechanism and treatment of acute lung injury caused by sepsis: research progress, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

When the patient suffers from sepsis, pulmonary capillary endothelium is damaged and vascular permeability increases. A large amount of protein-rich exudate destroys the barrier of pulmonary epithelial cells and accumulates in alveoli, which reduces effective ventilation and results in refractory hypoxemia, this is known as acute lung injury. Acute lung injury caused by sepsis is a common disease in intensive care unit, which has high hospital costs and high mortality. Meanwhile, it is also the focus of research on critical diseases. In this paper, the related literature were reviewed from four aspects, such as the mechanism of vascular endothelial injury, the mechanism of alveolar epithelial injury, the reduction of vascular endothelial injury and the protection of alveolar epithelium and the promotion of repair.

, correspAuthors=Xin-Bao Lian, authorNote=null, correspAuthorsNote=
*E-mail:
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脓毒症发生时肺毛细血管内皮损伤，血管通透性增加，大量富含蛋白质的渗出液破坏肺上皮细胞屏障并在肺泡内积聚，使有效通气减少，导致顽固性低氧血症，此即急性肺损伤。脓毒症急性肺损伤是重症监护病房的常见病，其住院花费大，病死率高，是危重症疾病研究的重点。该文主要从脓毒症急性肺损伤的血管内皮损伤机制、肺泡上皮损伤机制、减轻血管内皮损伤及保护肺泡上皮并促进修复四个方面对相关文献进行综述。

, correspAuthors=连新宝, authorNote=null, correspAuthorsNote=
连新宝，E-mail：
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张宇，医学硕士，主要从事中西医结合防治危重症方面的研究

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张宇，医学硕士，主要从事中西医结合防治危重症方面的研究

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张宇，医学硕士，主要从事中西医结合防治危重症方面的研究

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脓毒症急性肺损伤的发生机制及治疗研究进展
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张宇 , 卢笑晖 , 连新宝 *
解放军医学杂志 | 综述 2021,46(11): 1159-1164
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解放军医学杂志 | 综述 2021, 46(11): 1159-1164
脓毒症急性肺损伤的发生机制及治疗研究进展
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张宇, 卢笑晖, 连新宝*
作者信息
  • 山东中医药大学附属医院急诊/重症医学科，济南 250014

    • 张宇，医学硕士，主要从事中西医结合防治危重症方面的研究

通讯作者:

连新宝，E-mail：
Mechanism and treatment of acute lung injury caused by sepsis: research progress
Yu Zhang, Xiao-Hui Lu, Xin-Bao Lian*
Affiliations
  • Department of Emergency and Critical Care Medicine, Affiliated Hospital of Shandong University of Traditional Chinese Medicine,Jinan 250014, China
出版时间: 2021-11-28 doi: 10.11855/j.issn.0577-7402.2021.11.16
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摘要
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脓毒症发生时肺毛细血管内皮损伤，血管通透性增加，大量富含蛋白质的渗出液破坏肺上皮细胞屏障并在肺泡内积聚，使有效通气减少，导致顽固性低氧血症，此即急性肺损伤。脓毒症急性肺损伤是重症监护病房的常见病，其住院花费大，病死率高，是危重症疾病研究的重点。该文主要从脓毒症急性肺损伤的血管内皮损伤机制、肺泡上皮损伤机制、减轻血管内皮损伤及保护肺泡上皮并促进修复四个方面对相关文献进行综述。

脓毒症  /  急性肺损伤  /  血管内皮损伤  /  肺泡上皮损伤

When the patient suffers from sepsis, pulmonary capillary endothelium is damaged and vascular permeability increases. A large amount of protein-rich exudate destroys the barrier of pulmonary epithelial cells and accumulates in alveoli, which reduces effective ventilation and results in refractory hypoxemia, this is known as acute lung injury. Acute lung injury caused by sepsis is a common disease in intensive care unit, which has high hospital costs and high mortality. Meanwhile, it is also the focus of research on critical diseases. In this paper, the related literature were reviewed from four aspects, such as the mechanism of vascular endothelial injury, the mechanism of alveolar epithelial injury, the reduction of vascular endothelial injury and the protection of alveolar epithelium and the promotion of repair.

sepsis  /  acute lung injury  /  vascular endothelial injury  /  alveolar epithelial injury
张宇, 卢笑晖, 连新宝. 脓毒症急性肺损伤的发生机制及治疗研究进展. 解放军医学杂志, 2021 , 46 (11) : 1159 -1164 . DOI: 10.11855/j.issn.0577-7402.2021.11.16
Yu Zhang, Xiao-Hui Lu, Xin-Bao Lian. Mechanism and treatment of acute lung injury caused by sepsis: research progress[J]. Medical Journal of Chinese People’s Liberation Army, 2021 , 46 (11) : 1159 -1164 . DOI: 10.11855/j.issn.0577-7402.2021.11.16
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急性肺损伤(acute lung injury，ALI)是机体在严重感染、休克及创伤等情况下，肺毛细血管内皮细胞及肺泡上皮细胞(alveolar epithelial cell，AEC)损伤造成的非心源性肺水肿，临床主要表现为进行性的低氧血症及呼吸困难。ALI在重症监护病房最常见，一项流行病学调查纳入了我国44个重症监护病房的2322例脓毒症患者，结果显示68.2%的脓毒症患者合并ALI，90 d病死率达35.5%[1]。即使是好转出院的患者，在随后的两年甚至更长时间里，仍然继续遭受着危重病后遗症带来的痛苦，包括运动受限、心理后遗症、生活质量下降及经济负担等[2]。脓毒症ALI的病理变化主要包括早期炎性渗出、亚急性期组织化增生及晚期纤维化三个阶段[3]。经有效治疗后，大多数患者可出现炎症的消退及水肿的缓慢吸收即前两个阶段的表现[4]。如不进行早期干预，进展至脓毒症休克期时，肺组织灌注逐渐减少，肺毛细血管收缩，肺通气/灌注失衡加重，往往会对脏器造成不可逆的损害，甚至引起死亡[5]。脓毒症ALI的发病机制主要是血管内皮损伤、肺泡上皮损伤，对其治疗也主要从减轻血管内皮损伤及保护肺泡上皮并促进修复两方面开展。本文主要对脓毒症ALI的发病机制及治疗研究进展进行综述。
1 脓毒症ALI的发病机制
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1.1 血管内皮损伤的机制
脓毒症患者发生ALI时，多个分子相互作用以复杂的方式损伤肺血管内皮。血管内皮完整性是由血管内皮钙黏蛋白(VE-cadherin)与内皮受体激酶(Tie2)协同作用建立的，并受血管内皮蛋白酪氨酸磷酸酶(VE-PTP)的调控[6]，内皮反应元件结合蛋白(CREB)对VE-cadherin的转录及形成至关重要[7]。血管内皮细胞连接的稳定性是由产生张力的肌动蛋白细丝及产生拉力的肌动蛋白应激纤维共同决定的，二者在生理状态下保持着动态平衡[8]。脓毒症ALI还可引起肺、肾、肝组织微血管渗漏，组织中Angpt1(Ang1)、Tek(Tie2)、KDR(VEGFR2或Flk-1)基因表达下调，这些变化与上述基因上RNA聚合酶Ⅱ密度的降低有关，以肺组织中的反应最明显[9]。内皮细胞损伤还涉及炎症反应、细胞焦亡、氧化应激、细胞凋亡及自噬等多种途径。
1.1.1 炎症反应
细菌内毒素脂多糖(LPS)是导致脓毒症ALI急性炎症的主要刺激因子。LPS诱导脓毒症动物模型最为常用，微生物LPS通过辅助蛋白，如脂多糖结合蛋白(LBP)及分化簇14(CD14)与先天免疫细胞中由髓样分化蛋白2(MD2)及Toll样受体4(TLR4)组成的表面受体复合物结合。脂多糖TLR4/MD2复合物激活下游促炎信号通路，包括核因子-κB(NF-κB)激活多种促炎细胞因子的过度释放，导致急性细胞和(或)器官损伤，形成脓毒症ALI[10]。
1.1.2 细胞焦亡
全身暴露于LPS会导致严重的内皮细胞焦亡。这种焦亡由半胱氨酸蛋白酶(Caspases)家族介导，相关的蛋白有Caspase-1、4、5、11[11]。活化的Caspase-1切割Gasdermin D，使其形成Gasdermin D的N端或C端，Gasdermin D的N端与细胞膜上的磷脂蛋白结合，形成孔洞并将大量炎性因子释放到细胞外。Gasdermin D作为焦亡的直接执行蛋白，在血管内皮细胞损伤中起关键作用[12]。
1.1.3 氧化应激
氧化应激在脓毒症ALI中的作用已有较多文献报道。脓毒症炎症反应过程中释放了大量细胞因子及炎性细胞，通过氧化应激反应产生大量的活性氧自由基(ROS)，破坏细胞的结构及功能，尤其是可损伤线粒体功能[13]。核因子E2相关因子2(Nrf2)在细胞的防御与保护中起重要作用，具有抗氧化应激、抗炎及抑制细胞凋亡等作用。对脓毒症动物模型的研究发现，蛋白与C-激酶1(PICK1)可通过影响肺胱氨酸/谷氨酸转运体底物特异性亚单位XCT来调节肺血管内谷胱甘肽的合成，其机制是抑制Nrf2的激活[14]。
1.1.4 细胞凋亡及自噬
在脓毒症ALI血管内皮损伤过程中，自噬与凋亡处于一种对抗关系，Bcl-2家族蛋白是自噬与凋亡之间交互作用的调节因子。动物实验研究证实，经LPS处理后肺血管内皮细胞及肺组织细胞凋亡增加，吞噬功能增强，Bcl-2表达降低，Bad表达增加，PINK1/Parkin信号通路激活，而Bcl-2过表达及Bad基因敲除均可减轻LPS诱导的损伤，抑制细胞凋亡及有丝分裂，提高存活率；脓毒症可抑制肺组织中Beclin-1蛋白的表达，但不抑制Beclin-1 mRNA的表达，是典型的自噬激活[15]。
1.2 肺泡上皮损伤的机制
肺泡上皮细胞(AEC)由肺泡Ⅰ型(AT-Ⅰ)细胞及肺泡Ⅱ型(AT-Ⅱ)细胞组成。除气体交换外，肺泡液(AFC)的清除也是AEC的主要功能，AFC清除率与钠离子在肺泡上皮中通过顶端的上皮钠通道(ENaC)及基底外侧Na-K-ATPase的主动转运有关[16]。脓毒症ALI早期，肺泡基底膜发生局灶性破坏及剥脱，但细胞形态不发生变化，仅表现为上皮钙黏蛋白(E-cadherin)及β-连环蛋白(β-catenin)连接上的改变[4]。随后，肺血管内皮的通透性增加，液体及蛋白质聚集在肺间质内引起水肿，此时肺泡上皮的正常紧密屏障受损，随后水肿液被转移到肺泡内，其内包含的中性粒细胞数量及炎性趋化因子的激活程度与AEC损伤及ALI的严重程度密切相关[4]。丝裂原活化蛋白激酶(MAPK)信号通路在损伤过程中发挥重要作用，p38 MAPK通过激活Caspase-3及Caspase-7介导AEC的凋亡[17]，死亡相关蛋白激酶1(DAPK1)是一种促凋亡的钙调蛋白调节的丝氨酸/苏氨酸激酶，也参与了该过程[18]。在动物模型中AEC的脂肪酸氧化(FAO)明显受损，这种细胞的代谢缺陷可能是由于参与FAO及线粒体生物能量生成的关键介质[如过氧化物酶体增殖物激活受体γ共激活因子-1α (PGC-1α)、肉毒碱棕榈酰基转移酶1A(CPT1A)及中链酰基辅酶A(MCAD)]表达降低，使细胞处于易凋亡状态[19]。适度的自噬可保护细胞免受各种损伤，但过度的自噬尤其是在发病初期AT-Ⅱ细胞的自噬，则是ALI发生的主要原因之一，其潜在分子机制尚待进一步研究[20]。
2 脓毒症ALI的干预治疗
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2.1 减轻血管内皮损伤
炎症反应是肺血管内皮细胞损伤的主要原因，并与细胞焦亡、自噬及氧化应激等多个途径相互交错，TLR4介导的炎症信号通路也参与其中，因此，早期抑制炎症反应及保护血管内皮对脓毒症ALI的治疗尤为重要。
2.1.1 抑制炎症反应
从人脐血中分离的无限制体细胞(USSCs)[21]及口服非肽B1受体拮抗剂(BI113823)[22]均可抑制促炎细胞因子TNF-α、IL-6及抗炎细胞因子IL-10的水平，明显提高严重脓毒症大鼠的存活率，内源性子宫珠蛋白作为内源性抗炎信号在早期的ALI中也起到相似作用[23]。桥蛋白(OPN)是一种由免疫反应细胞产生的分泌型糖蛋白，在多种炎性疾病中起负面作用，经抗桥蛋白抗体(OPN Ab)处理的动物肺组织促炎细胞因子及趋化因子的mRNA及蛋白表达明显降低[24]，提示OPN也可能是治疗脓毒症ALI的潜在靶点。生长停滞及DNA损伤诱导蛋白34(Gadd34)的主要作用是调节内质网应激反应及细胞凋亡，体外实验表明，Gadd34可通过去磷酸化IKKβ抑制巨噬细胞产生促炎细胞因子，减轻LPS诱导的脓毒症及急性组织损伤[25]，而Gadd45β基因敲除(KO)脓毒症小鼠的早期肺细胞凋亡率明显增高，IL-1β、IL-6、IL-10及TNF-α等炎性因子表达明显升高，提示Gadd45β也具有肺保护作用[26]。瓜氨酸组蛋白H3(CitH3)参与了内皮细胞骨架的形成。有研究将最新研制的一种CitH3单克隆抗体用于靶向肽基精氨酸脱亚胺酶(PAD)2及PAD4产生的CitH3，发现其可减轻炎症反应，缓解ALI[27]。作为最具代表性的抗炎药物，糖皮质激素的使用一直备受争议。最新的一项双盲、单中心随机对照试验(RCT)结果显示，氢化可的松可明显改善早期脓毒症ALI患者的氧合指数及临床症状，但并不能改善患者的预后，其不良反应主要是血糖升高，但高血糖并不对预后产生影响[28]。动物实验表明3-羟基-3-甲基戊二酰辅酶A还原酶抑制剂(他汀类)能减轻肺损伤小鼠的炎症反应，临床研究也进一步证实辛伐他汀可通过降低肝素结合蛋白水平而改善患者预后[29]。但另一项临床RCT研究却显示瑞舒伐他汀并不能改善脓毒症ALI合并高炎症指标患者的预后[30]。
2.1.2 抑制TLR4介导的炎症信号通路
TLR4是一种表达于免疫细胞表面的先天免疫受体，其介导的信号通路参与了机体多种炎症反应。动物实验表明，多肽-金纳米颗粒杂化香烟烟雾提取物[31]、乌苯美司衍生物LYRM03[32]可通过抑制巨噬细胞中促炎性介质及MyD88依赖的TLR4信号转导通路，减轻其下游的炎症反应，有助于自噬诱导及随后的抗氧化蛋白表达，能有效减轻LPS诱导的ALI。烟酰胺腺嘌呤二核苷酸磷酸氧化酶2(NOX2)可抑制LPS诱导的脓毒症大鼠细胞因子表达、TLR通路信号转导及肺泡重塑，在新生儿脓毒症小鼠模型中同样有效[33]。靶向MD2的抑制剂阻断了TLR4信号通路的传导，可能是抑制急性炎症的潜在药物[34]。肉桂酰胺衍生物中有一种新的MD2抑制剂在体外可阻断LPS诱导的MD2/TLR4促炎信号的激活，减轻炎症反应[35]。有研究在分析黄腐酚与MD2分子对接的基础上，设计合成了39个含5碳连接链的双芳基-1，4-二烯-3-酮类化合物作为MD2抑制剂，可用于开发针对MD2的抗炎药[36]。姜黄素衍生的新型MD2抑制剂MAC17及MAC28的抗炎活性最强，对LPS刺激的巨噬细胞分泌细胞因子的抑制率达90%，具有肺保护作用[37]。
2.1.3 保护血管内皮
研究显示，p110γ在脓毒症ALI患者肺血管内皮细胞中的表达减弱，提示p110γ-FOXM1血管修复信号通路受损是肺血管内皮损伤及渗出液形成的关键因素，激活p110γ-FOXM1内皮细胞再生可能是修复血管的一种新策略[38]。糖酵解是内皮细胞(ECs)的主要生物能量途径，糖酵解激活剂PFKFB3在LPS处理的人肺动脉内皮细胞(HPAECs)及LPS攻击的小鼠肺内皮细胞中的表达及活性均明显增加，而内皮特异性PFKFB3基因敲除小鼠表现为内皮通透性降低、肺水肿减轻、存活率增高，提示抑制糖酵解具有肺保护作用[39]。研究显示，经雌激素相关受体(ERR)α的反向激动剂XCT-790处理的大鼠肺微血管内皮细胞(PMVECs)暴露于LPS后，内皮细胞通透性增加，紧密连接蛋白ZO-1、Occludin、JAM-A及VE-cadherin表达降低，而ERR的下调进一步加重了这些作用，沉默ERR基因也加剧了LPS诱导的炎性因子产生及NF-κB p65表达的增加，提示ERR作为一种新的负性调节因子在脓毒症ALI中发挥重要作用[40]。研究表明，重组人血栓调节蛋白可减轻肺毛细血管内皮细胞糖萼的损伤，与保留内皮细胞特异性分子1及硫酸乙酰肝素6-O-磺基转移酶1(内皮糖萼成分)的基因表达有关[41]，而巨噬细胞衍生的脂质介质MCTR1则可通过ALx/SIRT1/NF-κB/HPA途径减轻内皮细胞糖萼损伤，保护血管内皮[42]。
2.2 保护肺泡上皮并促进修复
2.2.1 保护肺泡上皮
A2B腺苷受体(A2BAR)具有保护AEC及减轻肺水肿的作用。一方面A2BAR通过抑制MAPK信号通路介导的线粒体凋亡途径减轻AEC损伤[17]；另一方面，A2BAR通过激活腺苷酸环化酶刺激cAMP的形成，促使ENaC提高AFC清除率，从而减轻肺水肿[43]。褪黑素也被证实可通过激活SIRT1/SGK1/Nedd4-2途径提高ENaC介导的AFC清除率，是一种新的治疗策略[44]。miR-34a是一种多功能调节剂，参与细胞增殖、凋亡、生长及自噬，可作为保护性因子抑制FoxO3表达，抑制AT-Ⅱ细胞过度的自噬活性，减轻对肺屏障的破坏[45]。
2.2.2 促进AEC修复
一旦AEC开始损伤，细胞将启动修复程序，该过程可能持续2~14 d，由于AT-Ⅰ细胞占肺泡上皮面积的95%以上，所以产生新的AT-Ⅰ细胞对于肺泡上皮修复至关重要，AT-Ⅱ细胞作为祖细胞可通过增殖分化形成AT-Ⅰ细胞，在严重损伤时，分泌细胞、支气管肺泡干细胞及角蛋白-5表达(KRT5+)细胞等均可替代祖细胞[46-47]。KRT5+细胞的增殖由缺氧诱导因子(HIF)-Notch及纤维细胞生长因子受体2信号转导驱动[48]，AT-Ⅱ细胞的增殖受Wnt-β-Catenin诱导，并被Notch及HIF79抑制[49]。FGF10-FGFR2B信号是维持AT-Ⅱ细胞必需的，可以在肺损伤后产生基底细胞，并通过支气管上皮干细胞促进AEC的再生[50]。Hippo-YAP信号通路通过磷酸化负调节其下游效应物YAP的转录活性，磷酸化的YAP在维持细胞增殖及凋亡稳态中起重要作用，还可调节AT-Ⅱ细胞的增殖[51]，同时YAP/TAZ蛋白也参与AT-Ⅱ向AT-Ⅰ分化[52]。黏着斑激酶(FAK)是一种细胞质蛋白酪氨酸激酶，通过FAK-PI3K-Akt途径促进了AEC的增殖及迁移，并阻止细胞凋亡，恢复肺泡的完整性[53]。随着干/祖细胞研究的进展，静脉输注骨髓间充质干细胞(MSCs)治疗脓毒症ALI的第1阶段临床试验显示患者耐受性良好[54]。有研究表明角质细胞生长因子(KGF)在ALI中可能是有益的[55]，但一项随机、双盲、安慰剂对照的第2阶段研究结果显示，KGF并不能改善患者的生理或临床结果，甚至可能是有害的[56]。
2.2.3 外泌体在AEC损伤修复中的作用
外泌体的直径为50~150 nm，是多囊泡核内体与母细胞胞膜融合后释放至胞外形成的，其内包含脂质、蛋白、受体、mRNA、lncRNA等成分，是细胞间信息传递的重要桥梁，目前已成为研究的热点。研究显示，MSCs分泌的外泌体包含MicroRNA-377-3p，后者可以通过靶向RPTOR调节自噬，抑制炎性因子，促进肺损伤的恢复[57]；而其包含的MicroRNA-30b-3p可下调SAA3的表达，从而减轻LPS诱导的AT-Ⅱ细胞损伤[58]。
2.2.4 机械通气与脓毒症ALI
呼吸机不能治疗脓毒症ALI，而是为肺屏障的修复及药物发挥作用争取时间。小潮气量、高呼气末正压(PEEP)的保护性通气策略是目前常用的方案，推荐使用初始小潮气量(6 ml/kg)。研究表明，初始潮气量每增加1 ml/kg，ICU死亡风险增加23%，与初始潮气量比较，随后的潮气量每增加1 ml/kg，死亡风险增加15%[59]。另一项研究显示，即使是保护性的通气策略，也可能会加重肺损伤[60]。既往曾报道高频振荡通气(HFOV)可以减少这种二次损伤发生，但研究发现其并不能降低30 d病死率[61]。更先进的通气模式，如气道压力释放通气(APRV)、使用时间控制的适应性通气(TCAV)方案可减轻肺损伤，其可能的机制包括改善肺泡不均匀性膨胀，减少肺泡、肺泡毛细血管的微应变及应力升高，减少肺泡潮气量，以及通过对抗腹内压的增加来调节胸腔内的压力[62]。
3 总结与展望
收起
血管内皮损伤和肺泡上皮损伤可从整体上概括脓毒症ALI的发病机制，但这其中包含了复杂的分子机制，尚待进一步研究证实。在治疗上，通过动物实验发掘潜在的抗炎药物的研究居多，临床试验相对较少。潜在的治疗药物从发现到临床应用是一个漫长的过程，部分动物实验研究提示有效，但临床试验却得到了相反的结果[29-30,56]。多途径靶向细胞移植(如间充质基质细胞)[56]及更优化的呼吸机通气模式[62]有望成为新的治疗选择，但仍须进一步临床研究进行验证。
基金
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  • 山东省中医药科技发展计划(2017-043)
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2021年第46卷第11期
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doi: 10.11855/j.issn.0577-7402.2021.11.16
  • 接收时间：2021-01-26
  • 首发时间：2025-12-19
  • 出版时间：2021-11-28
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  • 收稿日期：2021-01-26
  • 修回日期：2021-04-22
基金
Shandong Province Traditional Chinese Medicine Technology Development Plan(2017-043)
山东省中医药科技发展计划(2017-043)
作者信息
    山东中医药大学附属医院急诊/重症医学科，济南 250014

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https://castjournals.cast.org.cn/joweb/jfjyxzz/CN/10.11855/j.issn.0577-7402.2021.11.16
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2种不同金属材料的力学参数
科
Family		 属数
Number of
genus		 种数
Number of
species		 占总种数比例
Percentage of
total species (%)		 属
Genus		 种数
Number of
species		 占总种数比例
Percentage of total
species (%)
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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