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Article(id=1246531409230324333, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1246531406415941821, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.16.022, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1725206400000, receivedDateStr=2024-09-02, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1775125847394, onlineDateStr=2026-04-02, pubDate=1756310400000, pubDateStr=2025-08-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1775125847394, onlineIssueDateStr=2026-04-02, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1775125847394, creator=13701087609, updateTime=1775125847394, updator=13701087609, issue=Issue{id=1246531406415941821, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='16', pageStart='2251', pageEnd='2400', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1775125846723, creator=13701087609, updateTime=1775125956861, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1246531868481446285, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1246531406415941821, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1246531868481446286, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1246531406415941821, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=2374, endPage=2378, ext={EN=ArticleExt(id=1246531411402973827, articleId=1246531409230324333, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research progress on the regulation of pyroptosis by traditional Chinese medicine for the treatment of acute lung injury, columnId=1246531408630534361, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Acute lung injury (ALI) is a severe respiratory disease. Given the limited existing treatment methods, it is urgent to explore new therapies. Pyroptosis plays a crucial role in the onset of ALI. Traditional Chinese medicine can regulate the pathways related to pyroptosis, reduce the inflammatory response, and improve acute lung injury, thus providing new strategies for the treatment of ALI. This article systematically reviews the mechanisms by which pyroptosis causes ALI in alveolar macrophages, neutrophils, and pulmonary vascular endothelial cells, summarizes the published literature from 2019 to 2024, and explores the action mechanisms of active ingredients and compound prescriptions of traditional Chinese medicine in the treatment of ALI, aiming to provide a theoretical basis for the research and development of new drugs.

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急性肺损伤（ALI）是一种严重的呼吸系统疾病，而现有治疗手段有限，探寻新疗法迫在眉睫。细胞焦亡在ALI的发病中起关键作用，中医药可以通过调控细胞焦亡相关通路，减轻炎症反应，改善急性肺损伤，从而为治疗ALI提供新策略。本文通过系统梳理细胞焦亡在肺泡巨噬细胞、中性粒细胞、肺血管内皮细胞引发ALI的机制，归纳总结2019年至2024年已发表文献，探讨中药有效成分及复方在治疗ALI中的作用机制，旨在为新药研发提供理论依据。

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张志明，教授，主任医师，博士生导师 MP：13099267516 E-mail:
和建政，副教授，博士研究生导师 MP：17797520360 E-mail：
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赵冰（1992-），博士研究生，主要从事急危重症的中医药防治工作

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赵冰（1992-），博士研究生，主要从事急危重症的中医药防治工作

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赵冰（1992-），博士研究生，主要从事急危重症的中医药防治工作

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中医药调控细胞焦亡防治急性肺损伤的研究进展
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赵冰 1a , 李蓉蓉 1a , 徐倩 1a , 刘永琦 1b, 2 , 和建政 1b, 2 , 张志明 3
中国临床药理学杂志 | 综述 2025,41(16): 2374-2378
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中国临床药理学杂志 | 综述 2025, 41(16): 2374-2378
中医药调控细胞焦亡防治急性肺损伤的研究进展
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赵冰1a, 李蓉蓉1a, 徐倩1a, 刘永琦1b, 2, 和建政1b, 2 , 张志明3
作者信息
  • 1a.甘肃中医药大学 中医临床学院，甘肃　兰州　730000
  • 1b.甘肃中医药大学 基础医学院，甘肃　兰州　730000
  • 2.敦煌医学与转化教育部重点实验室，甘肃　兰州　730000
  • 3.甘肃省中医院，甘肃　兰州　730000

    • 赵冰（1992-），博士研究生，主要从事急危重症的中医药防治工作

通讯作者:

张志明，教授，主任医师，博士生导师 MP：13099267516 E-mail:
和建政，副教授，博士研究生导师 MP：17797520360 E-mail：
Research progress on the regulation of pyroptosis by traditional Chinese medicine for the treatment of acute lung injury
Bing ZHAO1a, Rong-rong LI1a, Qian XU1a, Yong-qi LIU1b, 2, Jian-zheng HE1b, 2 , Zhi-ming ZHANG3
Affiliations
  • 1a.Clinical College of Traditional Chinese Medicine, Gansu University of Chinese Medicine, Lanzhou 730000, Gansu Province, China
  • 1b.School of Basic Medicine, Gansu University of Chinese Medicine, Lanzhou 730000, Gansu Province, China
  • 2.Key Laboratory of Dunhuang Medicine and Transformation, Ministry of Education, Lanzhou 730000, Gansu Province, China
  • 3.Gansu Provincial Hospital of Chinese Medicine, Lanzhou 730050, Gansu Province, China
出版时间: 2025-08-28 doi: 10.13699/j.cnki.1001-6821.2025.16.022
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摘要
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急性肺损伤（ALI）是一种严重的呼吸系统疾病，而现有治疗手段有限，探寻新疗法迫在眉睫。细胞焦亡在ALI的发病中起关键作用，中医药可以通过调控细胞焦亡相关通路，减轻炎症反应，改善急性肺损伤，从而为治疗ALI提供新策略。本文通过系统梳理细胞焦亡在肺泡巨噬细胞、中性粒细胞、肺血管内皮细胞引发ALI的机制，归纳总结2019年至2024年已发表文献，探讨中药有效成分及复方在治疗ALI中的作用机制，旨在为新药研发提供理论依据。

中医药  /  急性肺损伤  /  细胞焦亡

Acute lung injury (ALI) is a severe respiratory disease. Given the limited existing treatment methods, it is urgent to explore new therapies. Pyroptosis plays a crucial role in the onset of ALI. Traditional Chinese medicine can regulate the pathways related to pyroptosis, reduce the inflammatory response, and improve acute lung injury, thus providing new strategies for the treatment of ALI. This article systematically reviews the mechanisms by which pyroptosis causes ALI in alveolar macrophages, neutrophils, and pulmonary vascular endothelial cells, summarizes the published literature from 2019 to 2024, and explores the action mechanisms of active ingredients and compound prescriptions of traditional Chinese medicine in the treatment of ALI, aiming to provide a theoretical basis for the research and development of new drugs.

traditional Chinese medicine  /  acute lung injury  /  pyroptosis
赵冰, 李蓉蓉, 徐倩, 刘永琦, 和建政, 张志明. 中医药调控细胞焦亡防治急性肺损伤的研究进展. 中国临床药理学杂志, 2025 , 41 (16) : 2374 -2378 . DOI: 10.13699/j.cnki.1001-6821.2025.16.022
Bing ZHAO, Rong-rong LI, Qian XU, Yong-qi LIU, Jian-zheng HE, Zhi-ming ZHANG. Research progress on the regulation of pyroptosis by traditional Chinese medicine for the treatment of acute lung injury[J]. Chinese Journal of Clinical Pharmacology, 2025 , 41 (16) : 2374 -2378 . DOI: 10.13699/j.cnki.1001-6821.2025.16.022
正文
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急性肺损伤（acute lung injury，ALI）是以肺部炎症、血管通透性增加和低氧性呼吸功能不全为特征的严重呼吸系统疾病，具有进展迅速、高发病率、高死亡率特点[1]，即使痊愈也会伴随不同程度焦虑、抑郁及创伤后应激障碍[2-3]，严重威胁人类的生命健康，也对医疗资源和社会经济造成极大挑战。目前治疗以机械辅助通气、抗炎及对症支持为主。因此，寻求有效的治疗药物显得尤为重要。细胞焦亡与ALI发病发展密切相关[4]，中医药能通过调控细胞焦亡相关信号通路而减轻炎症反应、改善组织损伤和促进组织修复。因此，本文通过总结中医药调控细胞焦亡治疗ALI的作用机制，以期为中医药治疗ALI及新药研发提供依据。
细胞焦亡（pyroptosis）是程序性细胞死亡的方式之一，Gasdermins（GSDMs）家族蛋白激活后释放的氮端结构域通过寡聚化并易位插入细胞膜形成膜孔，导致细胞肿胀、破裂及炎症级联反应[5]。依据所依赖的半胱氨酸蛋白酶（Caspase）的类型分为经典通路和非经典通路。经典途径与炎症小体的组装和Caspase-1的活化密切相关，当机体受到外源性刺激后，被细胞内的NOD样受体识别并通过凋亡相关斑点样蛋白（apoptosis-associated speck-like protein containing a CARD，ASC）与Pro-Caspase-1结合，活化Caspase-1裂解效应蛋白GSDMD，产生氮末端和碳末端，并介导白介素（interleukin，IL）-1β和IL-18释放，募集免疫细胞并刺激T细胞增殖，诱发炎症级联反应。非经典通路中，Caspase-4、-5、-11与脂多糖（lipopolysaccharide，LPS）在胞内结合，活化后裂解GSDMD诱导细胞焦亡，同时通过诱导钾离子流出激活核苷酸结合寡聚化结构域样受体蛋白3（NOD-like receptor protein 3，NLRP3）间接介导IL-1β和IL-18的成熟和释放[6]。
除Caspase家族蛋白参与焦亡外，中性粒细胞中的弹性蛋白酶和组织蛋白酶G可直接激活GSDMD，介导中性粒细胞焦亡[7]。此外，细胞毒性淋巴细胞中的颗粒酶Granzyme A能够水解肿瘤细胞中的GSDMB引起细胞焦亡[8]；自然杀伤细胞和细胞毒性T淋巴细胞中的颗粒酶Granzyme B能够直接切割GSDME，诱导肿瘤细胞焦亡[9]，这些发现为理解细胞焦亡的分子机制提供了新的视角。
1　细胞焦亡与ALI发生的关系
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1.1　肺泡巨噬细胞（alveolar macrophage，AM）焦亡
AM作为固有免疫中重要的效应细胞，能通过识别病原体相关分子模式和损伤相关分子模式激活炎症小体，AM焦亡诱导的过度炎症反应是ALI的关键[10]。在LPS引起的ALI中，通过Toll样受体4（toll-like receptor 4，TLR 4）/NLRP 3/Caspase-1途径诱发GSDMD依赖性AM焦亡，激活免疫细胞产生炎症因子，促进TLR 4表达和活性氧产生，导致血管间质水肿和中性粒细胞募集[11]，当TLR 4基因失活后ALI/急性呼吸窘迫综合征（acute espiratory distress syndrome，ARDS）减轻，因此，TLR 4是识别LPS炎症信号转导最重要的模式识别受体。在NLRP 3介导ALI的过程中，NLRP 3促进高迁移率族蛋白B1（high mobility group box 1，HMGB1）分泌而激活NLRP 3和Caspase-1，加剧AM焦亡，而通过抑制TLR 4/髓样分化因子88（myeloid differentiation primary response protein 88，MyD88）/核因子κB（nuclear factor kappa-B，NF-κB）信号通路阻断NLRP 3焦亡途径，ALI明显改善[12]。
1.2　中性粒细胞（neutrophils，NE）焦亡
在ALI发生早期，大量NE募集在肺部引起免疫过度激活，是引起炎症和肺损伤的主要原因，同时也与ALI/ARDS不良结局密切相关；而在损伤后期，NE通过吞噬细胞碎片、刺激组织血管生成等来促进肺组织修复[13]。近年来，研究发现中性粒细胞胞外陷阱（neutrophil extracellular traps，NETs）形成在ALI发病中起关键作用，NETs通过促进NLRP 3组装和Caspase-1/GSDMD的活化来介导脓毒症ALI小鼠AM 焦亡过程[14]，此外，还通过调节巨噬细胞极化来加速ALI发展。KOVACS等[15]发现，NE中Caspase-1和Caspase-11的活化都能裂解GSDMD蛋白，但只有Caspase-11活化时才能触发细胞焦亡，因此，NE焦亡可不依赖于Caspase-1介导，Caspase-11在该过程中可能发挥着更重要的作用。
1.3　肺血管内皮细胞（endothelial cells，EC）焦亡
EC为附着在肺微血管内壁的细胞，与细胞外基质、基底膜等共同构成肺内皮屏障，当机体受到外源性刺激时，EC出现广泛损伤和死亡，内皮屏障功能障碍对ALI演变及预后具有决定作用[16]。HUANG等[17]研究表明，EC内Caspase-11表达上调并激活GSDMD，通过NLRP 3/Caspase-1/GSDMD途径诱导EC焦亡，并抑制其增殖及血管壁修复。此外，CHENG等[18]研究表明，LPS可通过TLR 4/Caspase-11信号通路诱导小鼠EC焦亡，而当分别敲除Caspase-11和TLR 4时，前者细胞焦亡被抑制，后者未受影响，表明Caspase-11在EC焦亡中发挥重要作用。综上，细胞焦亡广泛参与ALI进程，其通过调控相关蛋白与基因表达，导致肺内皮屏障受损、炎性细胞浸润及肺泡通透性增加，因此，通过抑制细胞焦亡可能是今后治疗ALI的重要策略。
2　中医药调控细胞焦亡治疗ALI
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2.1　中药单体及活性成分
2.1.1　黄酮类
黄芩素（baicalin）是中药黄芩中含量最高的黄酮类化合物，具有抗炎、抗氧化、抗肿瘤等多种作用。研究表明，黄芩素能明显改善改善肺水肿、肺泡壁增厚与炎性细胞浸润，下调肺组织NLRP 3、ASC、cleaved Caspase-1和GSDMD-N表达，并减少血清和支气管肺泡灌洗液（bronchoalveolar lavage fluid，BALF）中IL-1β、肿瘤坏死因子（tumor necrosis factor-alpha，TNF-α）和IL-18水平，逆转细胞焦亡[19]。ZHANG等[20]研究显示，木犀草素能减少盲肠结扎穿孔致ALI大鼠血清和BALF中IL-1β、IL-6、TNF-α和IL-17A等炎症介质水平，下调Caspase-11、Caspase-1、GSDMD、IL-1α和IL-1β的蛋白表达水平，改善肺组织炎症。HAN等[21]研究表明，鸢尾素通过抑制热休克蛋白90/NLRP 3/Caspase-1/GSDMD信号通路，逆转巨噬细胞极化和减少焦亡，从而改善ALI。CAI等[22]的研究显示，葛根素通过下调组蛋白脱乙酰酶1（histone deacetylase 1，HDAC1），抑制蛋白磷酸酶2A/HDAC1/NLRP 3细胞焦亡通路改善ALI。
2.1.2　多酚/酚酸类
姜黄素具有抗炎、抗氧化及免疫调节等作用，能下调血清促炎因子、NF-κB及焦亡相关蛋白表达，上调肺组织沉默信息调节因子1，抑制焦亡来改善ALI[23]。LIU等[24]研究显示，和厚朴酚通过下调髓过氧化物酶、丙二醛、超氧化物歧化酶、IL-1β和IL-18，激活核因子-红细胞2相关因子2（nuclear factor erythroid 2-related factor 2，Nrf 2）抑制NLRP 3、ASC、Caspase-1、GSDMD表达而减轻ALI。ZHANG等[25]研究表明丁香树脂醇能降低肺组织和细胞中TNF-α、IL-6和IL-1β水平，靶向NLRP 3/GSDMD/Caspase-1通路抑制巨噬细胞焦亡。YANG等[26]研究证实马鞭草素通过激活G蛋白偶联受体18，减少NETs形成并靶向C/增强子结合蛋白δ（enhancer binding protein delta，EBP-δ）/GSDMD/GSDME轴抑制巨噬细胞焦亡来发挥治疗ALI的作用。
2.1.3　萜类
YAO等[27]研究证实，甘草酸能通过抑制NF-κB和丝裂活化蛋白激酶p38（mitogen activated protein kinase p38, p38)/细胞外信号调节激酶（extracellular signal regulated protein kinases, ERK)信号通路减少细胞因子（IL-6、TNF-α、IL 8、IL-1β和HMGB1）分泌、免疫细胞浸润（肺组织NEs和AMs）和细胞焦亡，从而显著缓解金黄色葡萄球菌感染所致的ALI。PU等[28]结合体内外实验研究了紫珠草二萜类化合物对ALI的作用，结果显示其通过阻断NLRP 3炎症小体活化来抑制J774A.1巨噬细胞焦亡，体内研究进一步揭示了其减少了CD 11b+ F4/80+巨噬细胞在肺部的浸润。PU等[29]研究表明去氢穿心莲内酯能同时通过PDPK 1泛素化阻断Akt/Nrf 2通路和NLRP 3介导的细胞焦亡，减缓ALI小鼠的炎症和氧化应激。
2.1.4　其他
蒽醌类成分大黄素能够下调ALI模型NLRP 3、ASC、Caspase-1、GSDMD抑制NLRP 3依赖的焦亡通路，减轻肺组织炎症[30]。生物碱类化合物苦豆碱[31]能明显减少IL-6、IL-8、受体相互作用蛋白激酶3（receptor-interacting protein kiuase 3, RIPK3)、丙酮酸脱氢酶复合物（pyruvate dehydrogenase complex，PDC）-E1α、PDC-E1β、PDC-E2、PDC-E3分泌，抑制细胞焦亡，减轻小鼠ALI。白芍总苷是白芍中提取的糖苷类化合物，戴胜凌等[32]实验证实白芍总苷能明显改善ALI大鼠肺组织病理性损伤及GSDMD-N和Caspase-1相对表达水平，从而抑制细胞焦亡。
2.2　中药复方/成药
2.2.1　清热宣肺类
PENG等[33]研究证实连花清咳片可通过抑制LPS诱导的NETs形成和细胞焦亡，减轻肺损伤和肺部炎症，在ALI/ARDS中发挥多重保护作用。HUANG[34]等建立冠状病毒ALI小鼠模型，发现清肺排毒汤能下调IL-1β、NLRP 3、ASC、Caspase-1、GSDMD和NF-κB的表达水平，且损伤改善程度呈剂量和时间依赖性，在保护组织完整性方面具有显著疗效。金茵清热口服液[35]能显著改善ALI小鼠肺组织病理学损伤，降低BALF中总蛋白水平，并抑制小鼠和RAW 264.7细胞NF-κB活化、促炎细胞因子水平及其下游蛋白NLRP 3、GSDMD表达，作用机制可能与下调NF-κB/NLRP 3/GSDMD通路有关。祖卡木颗粒[36]给药后，能显著抑制ALI小鼠血清中IL-10和IL-17A水平[对照组分别为(1364.99±33.40)、(154.45±3.04) pg·mL-1，模型组为(1397.45±150.15)、(167.35±2.46) pg·mL-1，祖卡木组为(1 571.27±127.77)和(159.36±3.52) pg·mL-1]，下调肺组织Caspase-1、GSDMD等蛋白表达[对照组分别为 (0.31±0.03)、(0.47±0.12) pg·mL-1，模型组为 (0.88±0.01)、(0.99±0.03) pg·mL-1，祖卡木组为(0.67±0.08)和(0.77±0.03) pg·mL-1]，从而改善ALI。
2.2.2　通腑泄热类
大承气汤出自东汉著名医家张仲景《伤寒论》，具有攻里通下、通腑泻热的作用，后世医家以此衍生出的宣白承气汤、柴芩承气汤等广泛应于临床。刘宇寒[37]研究了大承气汤预处理可降低ALI小鼠肺组织损伤评分、肺湿/干比、BALF中蛋白浓度及IL-6、IL-8、TNF-α、IL-18、IL-1β含量，抑制小鼠肺组织中 NLRP 3、Caspase-1、ASC、GSDMD的表达。宣白承气汤[38]和柴芩承气汤[39]均能明显改善ALI小鼠肺组织炎症损伤，下调TNF-α、IL-1β、IL-6的蛋白表达，而GSDMD介导的细胞焦亡是其抗ALI作用的核心靶点之一。
2.2.3　化瘀解毒类
ZHANG等[40]研究表明，血必净通过减少TNF-α、IL-6、IL-1β和TNF-α释放而保护肺泡上皮细胞免受GSDME介导的细胞焦亡，从而提高ALI小鼠存活率。MA等[41]研究表明，益气化瘀解毒方给药后ALI大鼠肺水肿明显减轻，血清IL-1β和IL-18水平降低，肺组织匀浆TLR 4从(971.02±84.30)降至(819.38±44.62) ng·mL-1，其抗炎作用可能与TLRP 4/NLRP 3信号通路的调节有关。LI等[42]实验表明，血府逐瘀汤可明显改善体外循环诱导ALI大鼠肺通气功能，并减轻肺组织损伤，下调NLRP 3、ASC、Caspase-1、p20、Pro-GSDMD、GSDMD p30、IL-18 mRNA或蛋白水平，可能机制为抑制肺内NF-κB/核因子κB抑制蛋白α（inhibitor of nuclear factor kappa-B alpha，IκB-α）通路减轻NLRP 3依赖性细胞焦亡。综上，中药复方通过调控细胞焦亡信号通路及相关蛋白，抑制炎症，改善肺组织损伤，发挥清热宣肺、通腑泄热、解毒活血而达到防治ALI的目的。
3　讨论
收起
通过归纳，表明中医药可通过抑制细胞焦亡信号通路及调控相关蛋白与基因表达，下调细胞因子而抑制炎症，减轻肺组织损伤，从而治疗ALI。中药有效成分集中在黄酮类、多酚类、萜类等化合物，复方以清热宣肺、通腑泻热和化瘀解毒为主，其调控机制多与NLRP 3炎症小体介导的NLRP 3/Caspase-1/GSDMD经典通路密切相关。尽管中医药治疗ALI目前取得一系列成果，然而，目前研究以动物实验为主，且ALI动物模型建立方法差别较大，而且，中医药作为中医理论指导下的治疗手段，关于中医辨证表观指标涉及较少，复方具有机制复杂、协同起效的特点，而以上研究基本集中在单一通路或机制。因此，在未来研究中需进一步探索建立统一的ALI建模标准或者病症结合模型，开展广泛临床试验，扩大中药单体及复方的研究范围，借助现代分子生物学技术深入探索细胞焦亡在ALI中的机制，以期为ALI治疗及药物研发提供新思路。
基金
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  • 国家自然科学基金地区项目(82460925)
  • 甘肃省联合科研基金重大项目(23JRRA1530)
  • 甘肃省科技重大专项-科技领军人才(21ZDKA0014)
  • 2025年度甘肃省研究生“创新之星”项目(2025CXZX-906)
文献
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2025年第41卷第16期
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doi: 10.13699/j.cnki.1001-6821.2025.16.022
  • 接收时间：2024-09-02
  • 首发时间：2026-04-02
  • 出版时间：2025-08-28
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  • 收稿日期：2024-09-02
基金
国家自然科学基金地区项目(82460925)
甘肃省联合科研基金重大项目(23JRRA1530)
甘肃省科技重大专项-科技领军人才(21ZDKA0014)
2025年度甘肃省研究生“创新之星”项目(2025CXZX-906)
作者信息
    1a.甘肃中医药大学 中医临床学院，甘肃　兰州　730000
    1b.甘肃中医药大学 基础医学院，甘肃　兰州　730000
    2.敦煌医学与转化教育部重点实验室，甘肃　兰州　730000
    3.甘肃省中医院，甘肃　兰州　730000

通讯作者:

张志明，教授，主任医师，博士生导师 MP：13099267516 E-mail:
和建政，副教授，博士研究生导师 MP：17797520360 E-mail：
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species		 占总种数比例
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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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