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Article(id=1208073010330833728, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208073005197009056, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.2022.05.0518, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1620403200000, receivedDateStr=2021-05-08, revisedDate=null, revisedDateStr=null, acceptedDate=1624291200000, acceptedDateStr=2021-06-22, onlineDate=1765956650574, onlineDateStr=2025-12-17, pubDate=1653667200000, pubDateStr=2022-05-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1765956650574, onlineIssueDateStr=2025-12-17, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1765956650574, creator=13701087609, updateTime=1765956650574, updator=13701087609, issue=Issue{id=1208073005197009056, tenantId=1146029695717560320, journalId=1189873630562394117, year='2022', volume='47', issue='5', pageStart='427', pageEnd='532', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1765956649350, creator=13701087609, updateTime=1765956710955, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1208073263641633510, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208073005197009056, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1208073263641633511, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208073005197009056, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=518, endPage=523, ext={EN=ArticleExt(id=1208073010687349585, articleId=1208073010330833728, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Research progress in the relationship of autophagy and blood brain barrier, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Autophagy has a certain degree of protective effect on cells, but excessive autophagy can lead to programmed cell death, which is called Ⅱ programmed cell death. The blood brain barrier (BBB) plays a protective role between the brain and the peripheral circulation, which helps the inflow and outflow of molecules and ions to maintain the steady state of the central nervous system. A large number of studies have shown that autophagy plays an important role in BBB dysfunction, on the one hand, autophagy can damage or protect the integrity of BBB, and on the other hand, autophagy can also affect the passage of drugs,pathogens and other substances through BBB. Therefore, regulating autophagy level by targeting specific regulatory molecules in autophagy mechanism may affect the function of BBB, and then affect the occurrence and development of central nervous system diseases. The recent advances in the relationship between autophagy and BBB have been reviewed in present paper for hoping to provide new ideas for the prevention and treatment of diseases related to BBB injury.

, correspAuthors=Xiao-Min Wang, authorNote=null, correspAuthorsNote=
*E-mail:
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自噬对细胞具有一定的保护作用，但过度自噬则会导致细胞程序性死亡，称为Ⅱ型程序性细胞死亡。血脑屏障(BBB)在大脑与外周循环之间起保护作用，有助于分子和离子的流入和流出，以维持中枢神经系统的稳态。大量研究表明，细胞自噬在BBB功能中发挥着重要作用，一方面可对BBB的完整性起到损伤或保护作用，另一方面可影响药物、病原体等物质穿越BBB。因此，通过靶向自噬机制中的特定调节分子来调节自噬水平可能影响BBB的功能，进而影响中枢神经系统疾病的发生和发展。本文对细胞自噬与BBB之间关系的研究进展进行综述，以期为预防和治疗BBB损伤相关的疾病提供新思路。

, correspAuthors=王小敏, authorNote=null, correspAuthorsNote=
王小敏，E-mail：
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王俣棋，硕士研究生，主要从事链球菌穿越血脑屏障机制方面的研究

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王俣棋，硕士研究生，主要从事链球菌穿越血脑屏障机制方面的研究

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王俣棋，硕士研究生，主要从事链球菌穿越血脑屏障机制方面的研究

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细胞自噬与血脑屏障的关系研究进展
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王俣棋 , 徐鹏 , 范红结 , 王小敏 *
解放军医学杂志 | 综述 2022,47(5): 518-523
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解放军医学杂志 | 综述 2022, 47(5): 518-523
细胞自噬与血脑屏障的关系研究进展
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王俣棋, 徐鹏, 范红结, 王小敏*
作者信息
  • 遵义医科大学基础医学院，贵州遵义 563000

    • 王俣棋，硕士研究生，主要从事链球菌穿越血脑屏障机制方面的研究

通讯作者:

王小敏，E-mail：
Research progress in the relationship of autophagy and blood brain barrier
Yu-Qi Wang, Peng Xu, Hong-Jie Fan, Xiao-Min Wang*
Affiliations
  • School of Basic Medicine, Zunyi Medical University, Zunyi, Guizhou 563000, China
出版时间: 2022-05-28 doi: 10.11855/j.issn.0577-7402.2022.05.0518
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摘要
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自噬对细胞具有一定的保护作用，但过度自噬则会导致细胞程序性死亡，称为Ⅱ型程序性细胞死亡。血脑屏障(BBB)在大脑与外周循环之间起保护作用，有助于分子和离子的流入和流出，以维持中枢神经系统的稳态。大量研究表明，细胞自噬在BBB功能中发挥着重要作用，一方面可对BBB的完整性起到损伤或保护作用，另一方面可影响药物、病原体等物质穿越BBB。因此，通过靶向自噬机制中的特定调节分子来调节自噬水平可能影响BBB的功能，进而影响中枢神经系统疾病的发生和发展。本文对细胞自噬与BBB之间关系的研究进展进行综述，以期为预防和治疗BBB损伤相关的疾病提供新思路。

自噬  /  血脑屏障  /  病原体  /  药物

Autophagy has a certain degree of protective effect on cells, but excessive autophagy can lead to programmed cell death, which is called Ⅱ programmed cell death. The blood brain barrier (BBB) plays a protective role between the brain and the peripheral circulation, which helps the inflow and outflow of molecules and ions to maintain the steady state of the central nervous system. A large number of studies have shown that autophagy plays an important role in BBB dysfunction, on the one hand, autophagy can damage or protect the integrity of BBB, and on the other hand, autophagy can also affect the passage of drugs,pathogens and other substances through BBB. Therefore, regulating autophagy level by targeting specific regulatory molecules in autophagy mechanism may affect the function of BBB, and then affect the occurrence and development of central nervous system diseases. The recent advances in the relationship between autophagy and BBB have been reviewed in present paper for hoping to provide new ideas for the prevention and treatment of diseases related to BBB injury.

autophagy  /  blood-brain barrier  /  pathogen  /  drug
王俣棋, 徐鹏, 范红结, 王小敏. 细胞自噬与血脑屏障的关系研究进展. 解放军医学杂志, 2022 , 47 (5) : 518 -523 . DOI: 10.11855/j.issn.0577-7402.2022.05.0518
Yu-Qi Wang, Peng Xu, Hong-Jie Fan, Xiao-Min Wang. Research progress in the relationship of autophagy and blood brain barrier[J]. Medical Journal of Chinese People’s Liberation Army, 2022 , 47 (5) : 518 -523 . DOI: 10.11855/j.issn.0577-7402.2022.05.0518
正文
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自噬是一种高度保守的生物学现象，在大多数细胞中，基础水平的自噬不断发生。自噬能够清除错误折叠的蛋白质和受损的细胞器，这对于细胞在各类应激状态下的存活及保持自身完整性至关重要[1-2]。研究表明，自噬参与调节先天性免疫和获得性免疫，与机体健康密切相关，自噬流受阻可能导致癌症、亨廷顿病、帕金森病等疾病[3-4]。血脑屏障(blood brain barrier，BBB)在大脑与外周循环之间起保护作用，主要由脑微血管内皮细胞(cerebral microvascular endothelial cells，BMECs)、周细胞、星形胶质细胞和神经元组成，其中BMECs通过紧密连接(tight junction，TJ)蛋白连接[5-6]。TJ蛋白是BBB控制脑血管通透性的主要功能成分，BBB功能障碍通常与内皮细胞紧密连接的破坏或过度通透有关，可导致各种中枢神经系统疾病。因此，维持BBB结构的完整性和正常功能对中枢神经系统的稳态和生理功能至关重要。最近研究表明，细胞自噬过程受一系列生物因子和化合物的调节，且可能对BBB的功能与结构完整性产生重大影响。本文综述目前关于细胞自噬在BBB完整性、防止病原体等有害物质穿越BBB、加速药物穿越BBB进而发挥药效等方面的研究进展，旨在为进一步探讨自噬与中枢神经系统疾病的关系奠定理论依据。
1 自噬与BBB相互影响
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自噬对BBB有着双重作用，在某些情况下，自噬对BBB的完整性起到保护作用，主要表现在缺血缺氧等应激状态下有助于维持BBB的完整性以及脑损伤后对BBB的修复作用。然而，有研究表明，自噬对BBB的完整性亦可起到损伤或破坏作用[7]。
1.1 细胞自噬对BBB的保护作用
大多数情况下，自噬具有保护细胞的作用，自噬对BBB的有益作用与自噬如何被诱导以及自噬发生在何种细胞内相关。当细胞营养被剥夺或处于缺氧状态下，自噬被激活并对紧密连接蛋白-5(claudin-5)进行再分配，claudin-5是BBB形成紧密连接的关键分子，可以封闭细胞间隙并维持细胞旁屏障[8]，从而维持BBB正常的生理功能[9-10]。Engelhardt等[11]探究BBB相关细胞在缺血缺氧条件下的反应差异时发现，周细胞和星形胶质细胞可通过激活自噬途径来调控其自身的存活，由此推测，自噬可能是周细胞和星形胶质细胞对缺血缺氧损伤的一种适应性手段，其机制是通过分解现有的细胞质前体促进受损线粒体的清除和三磷酸腺苷(adenosine triphosphate，ATP)的再生，但仍需深入研究其潜在机制。
一些化合物诱导的自噬对BBB具有保护和修复作用。例如，葡萄糖代谢过程中产生的反应性代谢产物甲基乙二醛引起的自噬可保护BMECs免受损伤，有助于维持BBB的完整性[12]；黄芩苷是一种神经保护剂，可减轻脑水肿，从而减轻BBB的破坏，其神经保护机制亦是通过激活自噬因子实现的[13]；富含橄榄油的特级初榨橄榄油(extra-virgin olive oil，EVOO)改善BBB的紧密性也是通过激活腺苷酸活化蛋白激酶(AMP-activated protein kinase，AMPK)途径诱导自噬实现的[14]。
自噬可减轻脑损伤引起的BBB破坏。木犀草素是类黄酮家族的一员，被证实在创伤性脑损伤(traumatic brain injury，TBI)后可激活自噬，减少促炎因子IL-1β和TNF-α的mRNA和蛋白表达量，减轻神经元变性，进而减轻TBI引发的脑水肿和对BBB的破坏[15]。相反，一些对BBB有害的物质通过抑制自噬而发挥损伤BBB的作用。研究发现，肿瘤坏死因子受体相关因子6通过抑制自噬和促进氧化应激而加重蛛网膜下腔出血，加重早期脑损伤程度，而早期脑损伤主要包括BBB损伤、神经元死亡和脑水肿[16]。
1.2 细胞自噬对BBB的损伤作用
自噬也可损伤BBB相关细胞，在这种情况下，抑制自噬反而可保护BBB的完整性。最近研究证实，人类免疫缺陷病毒1型(human immunodeficiency virus-1，HIV-1)编码的反式转录激活因子(transactivator of transcription，TAT)蛋白破坏BBB的紧密连接是通过诱导自噬实现的[17]。此外，血管基底膜外周细胞的存在对于维持BBB的完整性至关重要，而自噬是周细胞凋亡的上游过程。因此，通过sigma-1受体激动剂抑制自噬可明显提高周细胞存活率，维持BBB的完整性[18-22]。氧糖剥夺(oxygen–glucose deprivation，OGD)诱导的自噬可导致脑内皮细胞功能障碍、BBB通透性增加[23]。Wu等[24]探讨了线粒体分裂抑制剂1(Mdivi-1)在TBI后的自噬和线粒体自噬中的潜在作用机制，发现Mdivi-1可减缓TBI介导的BBB破坏和细胞死亡，且部分是通过抑制异常自噬和激活线粒体自噬实现的。
一氧化氮(NO)、小凹蛋白1(caveolin-1)与自噬体相互作用，在长时间缺血条件下可诱导claudin-5降解，破坏BBB的完整性，其部分机制是NO作为一个触发器，可促进caveolin-1将claudin-5传递给自噬体，随后被溶酶体降解[25]。研究发现，硫化氢供体(NaHS)可抑制自噬，保护神经元免受凋亡，促进髓鞘化和轴突修复，维持BBB的完整性[26]。同样，dl-3-正丁基苯酞(dl-3n-butylphthalide，Dl-NBP)也可通过抑制自噬而阻断TJ蛋白丢失和神经元凋亡，发挥保护BBB的作用[27]。在体内试验中，OGD诱导90 min后，再灌注16 mmol/L葡萄糖30 min，结果显示高糖可显著诱导自噬，加重BBB损伤；同样，采用自噬激活剂雷帕霉素增强自噬可进一步导致紧密连接蛋白1(zonula oc-cludens-1，ZO-1)表达降低或再分配，从而增加BBB的通透性[28]。3xTg-AD小鼠脑血管、胰岛素受体-β(insulin receptor-beta，IR-β)和低密度脂蛋白受体相关蛋白-1(lipoprotein receptor-related protein-1，LRP-1)水平降低与自噬标记微管相关蛋白1轻链3(light chain 3，LC3)水平升高相关，但IR-β和LRP-1也在形成BBB的脑毛细血管内皮细胞(brain capillary endothelial cells，BCEC)中表达，提示自噬可能参与破坏BBB[29]。
1.3 BBB诱导细胞自噬
一些病原菌或有害物质损伤BBB时，BBB本身可能会通过某些途径诱导自噬。B群链球菌(group B Streptococcus，GBS)感染期间，BBB内皮细胞激活的自噬有助于限制内皮细胞内微生物的生长和繁殖[30]。砷对于发育中的大脑具有神经毒性，砷暴露可引起BBB通透性增加，Manthari等[31]在不同周龄小鼠的饮用水中加入不同剂量的三氧化二砷，发现TJ蛋白(Occludin、Claudin、ZO-1和ZO-2)、磷脂酰肌醇-3-激酶(phosphatidylinositol-3-kinase，PI3K)、蛋白激酶B(Akt)、哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin，mTOR)及p62的mRNA表达水平明显降低，Occludin蛋白表达水平明显降低，Beclin1、LC3-Ⅰ、LC3-Ⅱ、Atg5和Atg12的mRNA和蛋白表达水平升高；透射电镜超微结构分析显示，在产后21 d和42 d，高剂量砷暴露小鼠的大脑皮质和海马出现自噬小体和空泡化轴突。以上结果表明，大脑皮质和海马中不完整的BBB可能通过抑制PI3K/Akt/mTOR信号通路且以周龄依赖的方式促进砷的转移并诱导自噬。但BBB诱导的自噬是否有助于增强宿主细胞的防御作用尚待进一步研究证实。
2 缺血性脑损伤中自噬对BBB的作用
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在缺血性脑损伤时发生的自噬对BBB发挥着双重作用，包括保护作用和损伤作用，具体发挥哪种作用取决于自噬的发生情况、研究对象的患病情况以及对研究对象进行的基因编辑。
2.1 脑缺血再灌注损伤时诱导的BMECs自噬对BBB的保护作用
脑缺血再灌注(ischemia reperfusion，I/R)引起的BMECs损伤是BBB破坏的初始阶段，可导致缺血性脑卒中患者预后不良。研究证实，缺血性脑卒中时的自噬BMECs具有保护作用[32]。例如，长链非编码RNA MALAT1可通过增强BMECs的自噬发挥保护BBB的作用，其机制是MALAT1直接与miR-26b结合，下调miR-26b的表达，进而逆转miR-26b对BMECs自噬和存活的抑制作用，参与促进miR-26b靶蛋白ULK2的表达[33]。Shi等[34]发现，沉默组蛋白去乙酰化酶9(histone deacetylase 9，HDAC9)基因可减轻脑卒中时的脑损伤，进一步分析显示，HDAC9可加重脑缺血再灌注损伤时的BMECs损伤。此外，研究人员进一步发现，HDAC9能够抑制自噬，且与内皮细胞功能障碍有关。上述结果表明，脑缺血再灌注损伤时沉默HDAC9基因可促进自噬，这对BBB通透性具有保护作用。
2.2 缺血性脑损伤时自噬对BBB的损伤作用
自噬因氧和葡萄糖被剥夺而增强，BBB成分claudin-5被脑血管内皮细胞的自噬溶酶体降解，表明自噬能够加重BBB损伤[15]。Wei等[35]基于自噬抑制功能恢复的观察结果证实，糖尿病小鼠脑缺血期间自噬增强是导致BBB过度破坏的原因。在NF-JB p50基因敲除小鼠中观察到自噬和BBB损伤增加，抑制自噬可逆转这些现象，且自噬可调节核因子κB导致的缺血性神经元和血管损伤[36]。
3 自噬在细菌感染BBB中的作用
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3.1 自噬调节BBB细胞防御机制阻止GBS入侵和产毒
Cutting等[30]发现，GBS感染导致GFP-LC3点状分布增加，内源性LC3-Ⅱ和p62周转水平增高，这是主动自噬通量的两个标志性指标，证实GBS感染可诱导自噬。感染GBS突变株实验发现，GBS侵袭和GBS打孔β-溶血素/细胞溶素(β-hemolysin/cytolysin，β-h/c)能够激活自噬，GBS脑膜炎小鼠模型进一步证实了该结果，野生型GBS感染在脑组织中诱导的自噬水平高于β-h/c缺失突变体，使用ATG5敲除的成纤维细胞抑制自噬或siRNA介导的人脑微血管内皮细胞(human brain microvascular endothelial cells，hBMECs)自噬障碍都会促进细胞内GBS数量的恢复，然而，电镜观察结果显示，尽管可见到GBS-LC3共定位，但在双膜自噬结构中仅能观察到少量的GBS，表明虽然自噬可以调节BBB细胞防御阻止GBS入侵和产毒，但GBS能够积极地阻止自噬途径以促进自身繁殖。
3.2 自噬在炭疽杆菌感染hBMECs中的作用
炭疽脑膜炎的发生是由于炭疽杆菌能够穿越BBB，其感染主要取决于两种炭疽毒素的表达，即致死毒素和水肿毒素。有研究发现，炭疽毒素的表达能够诱导宿主hBMECs产生自噬，抑制炭疽杆菌在细胞内的存活。因此，当机体感染炭疽杆菌时，自噬在某种程度上起到免疫保护作用[37]。
3.3 自噬在大肠埃希菌K1感染hBMECs中的作用
在大肠埃希菌K1侵袭hBMECs的过程中，hBMECs自噬水平增高可以降低细胞内细菌的存活率。研究发现，烟草烟雾中的核心成分尼古丁可通过激活NF-κB和PI3K/Akt/mTOR信号通路来抑制大肠埃希菌K1感染诱导的hBMECs自噬，导致BBB受损，增高新生儿脑膜炎的发病率[38]。
4 自噬参与药物、毒素穿越BBB而发挥作用
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4.1 自噬参与药物穿越BBB
细胞自噬是一种保守的依赖溶酶体的降解途径，作为一种细胞保护机制，其在多种肿瘤细胞中可引起治疗抗性[39-40]。研究发现，羟基氯喹可以抑制自噬过程中自噬体与溶酶体的结合，从而增强酪氨酸激酶抑制剂ZD6474的抗胶质瘤作用。然而，ZD6474在体内的非选择性分布和羟基氯喹穿越BBB时的低穿透能力限制了其在胶质瘤治疗中的临床应用。研究人员将ZD6474和羟基氯喹共同包入R6dGR肽修饰的脂质体(R6dGR peptide-modified liposomes，R6dGR-Lip)中，明显提高了羟基氯喹穿越BBB的能力。因此，R6dGR-Lip负载羟基氯喹能够更有效地阻断胶质瘤细胞的自噬通量，从而发挥ZD6474对胶质瘤的治疗作用[41]。紫外线吸收剂二苯甲酮-3(benzophenone-3，BP-3)是各种个人护理用品中使用最广泛的化学物质。研究表明，小鼠出生前暴露于BP-3(使用环境相关剂量)会损害自噬体和自噬相关因子，同时BP-3对BBB具有良好的渗透性，但是自噬在BP-3穿越BBB中的作用仍需要进一步探讨[42]。
4.2 自噬参与毒素穿越BBB
T-2毒素是由多种真菌产生的单端孢霉烯族毒素之一，是食品和动物饲料中常见的污染物，也存在于加工过的谷物产品中，具有神经毒性作用。T-2毒素可在体内通过BBB，引起脑损伤和垂体损伤。研究发现，在T-2毒素处理后，大鼠脑内存在明显的自噬现象，且垂体细胞凋亡明显，表明T-2毒素的神经毒性作用与其能够穿越BBB以及自噬过程有关[43]。
5 自噬调节剂穿越BBB用于疾病的治疗
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5.1 自噬抑制剂穿越BBB用于疾病的治疗
自噬是一种依赖于溶酶体降解和细胞存活的过程，由于其在DNA损伤中的作用而成为癌症治疗的新靶点[44]。研究表明，抑制自噬可以提高肿瘤细胞的放射敏感性[40,45-46]。目前，自噬抑制剂已被证实能够提高放射性治疗胶质母细胞瘤(glioblastoma，GBM)的疗效[47]。然而由于BBB的存在，大多数自噬抑制剂并不能有效地使GBM患者受益。有研究发现，三氟拉嗪(trifluoperazine，TFP)能够干扰溶酶体的酸化，抑制自噬。此外，TFP可抑制P糖蛋白(P-glycoprotein，P-gp)的表达，这可能有助于药物进入大脑和GBM中，从而发挥作用。此外，TFP治疗削弱了放射治疗后DNA损伤的修复，为TFP联合放射治疗GBM提供了理论依据[48-49]。
5.2 自噬诱导剂穿越BBB用于疾病的治疗
研究人员设计并合成了Qu修饰的P-80稳定AuPd核壳结构(Qu@P-80@AuPd)，作为自噬诱导剂，其可加速清除细胞内的β淀粉样蛋白(amyloid-β，Aβ)，保护细胞免受Aβ诱导的损伤，并有效地通过BBB。因此，Qu@P-80@AuPd可能成为治疗阿尔兹海默病的潜在自噬诱导剂[50]。此外，最近研究表明，自噬促进剂雷帕霉素可作为治疗阿尔兹海默病药物的成分之一，能够穿越BBB在病灶处发挥重要作用：可通过促进细胞自噬加速Aβ和磷酸化Tau蛋白的降解，还可通过抑制NO的合成减轻阿尔兹海默病病灶的炎症，减轻氧化应激反应，在阿尔兹海默病的治疗中发挥重要作用[51]。
6 总结与展望
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自噬在BBB生理学和相关疾病中的重要作用逐渐受到关注，然而自噬在BBB中的确切生物学效应和潜在机制尚未阐明，针对自噬对BBB受损后的修复治疗策略仍然处于假设阶段。近年来，细胞的自噬效应引起了人们极大的兴趣，越来越多的数据证实细胞自噬与BBB关系密切，两者相互影响、相互作用。BBB可诱导细胞自噬，调节BBB相关细胞的损伤。脑缺血可导致细胞自噬的发生，细胞自噬适度激活有利于BBB相关细胞的修复，但是细胞自噬激活过度或不足亦可导致细胞凋亡，加重BBB损伤。同时，细胞自噬在防止病原体等有害物质穿越BBB、加速药物穿越BBB发挥作用等方面也起着重要作用。因此，合理利用自噬这把“双刃剑”将有助于治疗和预防BBB损伤相关的多种神经系统疾病，并为肿瘤等疾病的治疗提供新思路。
基金
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  • 国家自然科学基金地区科学基金项目(31860706)
  • 贵州省教育厅青年科技人才成长项目(黔教合KY字[2018]222)
  • 国家级大学生创新创业项目(202010661004)
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2022年第47卷第5期
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doi: 10.11855/j.issn.0577-7402.2022.05.0518
  • 接收时间：2021-05-08
  • 首发时间：2025-12-17
  • 出版时间：2022-05-28
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  • 收稿日期：2021-05-08
  • 录用日期：2021-06-22
基金
National Natural Science Foundation of China(31860706)
国家自然科学基金地区科学基金项目(31860706)
Young Scientific and Technological Talents Growth Project of Guizhou Provincial Education Department(KY[2018]222)
贵州省教育厅青年科技人才成长项目(黔教合KY字[2018]222)
National Undergraduate Innovation and Entrepreneurship Project(202010661004)
国家级大学生创新创业项目(202010661004)
作者信息
    遵义医科大学基础医学院，贵州遵义 563000

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王小敏，E-mail：
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2种不同金属材料的力学参数
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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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