Article(id=1322926012182438090, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322925862630339452, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2025.07.025, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=null, receivedDateStr=null, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1793339740081, onlineDateStr=2026-10-30, pubDate=1752076800000, pubDateStr=2025-07-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1793339740081, onlineIssueDateStr=2026-10-30, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1793339740081, creator=13701087609, updateTime=1793339740081, updator=13701087609, issue=Issue{id=1322925862630339452, tenantId=1146029695717560320, journalId=1255847919539208197, year='2025', volume='43', issue='7', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1752076800000', pubDateStr='2025-07-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1793339704424, creator='13701087609', updateTime=1793340532184, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1322929334587105328, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322925862630339452, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1322929334587105329, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322925862630339452, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=114, endPage=120, ext={EN=ArticleExt(id=1322926012379570379, articleId=1322926012182438090, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Research Progress on Pharmacological Action and Mechanism of Cangzhu(Atractylodis Rhizoma), columnId=1256183361521967297, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Target on National Project, runingTitle=null, highlight=null, articleAbstract=

Cangzhu(Atractylodis Rhizoma)is a major traditional Chinese medicine commonly used in TCM clinical practice and has a long history of medicinal use. It has the effect of drying dampness and strengthening spleen,dispelling wind and dispelling cold,and brightening eyes. It is widely used in gastrointestinal diseases and rheumatic diseases,the clinical effect is remarkable. The main active ingredients are volatile oils,including atractyloketone,atractylotin,β-phylloalcohol and citronol. Atractylotin is one of the main efficacy components of Cangzhu(Atractylodis Rhizoma). It is also an important index component for quality control of Cangzhu(Atractylodis Rhizoma). Modern pharmacological studies have shown that atractylotin has anti-inflammatory,gastric emptying,anti-tumor,positive muscle strength,antibacterial,liver protection,heart protection,antioxidant activities. It has a wide range of anti-inflammatory effects and therapeutic effects on intestinal inflammation,arthritis,airway inflammation,pneumonia,etc. It can improve gastrointestinal function to strengthen spleen,inhibit the proliferation of bile duct cancer,liver cancer,breast cancer and lung cancer cells,and has significant antibacterial effect. The liver protection effect may be related to its antioxidant and anti-inflammatory activities,and it also has protective effects on the heart and nervous system. Atractylotin has a wide range of pharmacological effects and great potential for development and application. With further research,more and more pharmacological mechanisms will be elucidated,which will play an important role in promoting the development and utilization of atractylotin. The pharmacological action and mechanism of atractylotin were summarized in order to provide reference for its clinical application and new drug development.

, authors=Ping YANG, Xixiang LI, Wei SONG, Xuemei WANG, authorsList=Ping YANG, Xixiang LI, Wei SONG, Xuemei WANG, authorCompany=null, correspAuthors=Xixiang LI, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1322926017362403554, articleId=1322926012182438090, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=苍术素药理作用及机制的研究进展, columnId=1256183362172142382, journalTitle=中华中医药学刊, columnName=国家项目点击, runingTitle=null, highlight=null, articleAbstract=

苍术为中医临床常用的大宗中药,药用历史悠久,具有燥湿健脾、祛风散寒、明目的功效,在胃肠道疾病、风湿性疾病中应用广泛,临床疗效显著。主要活性成分为挥发油类,包括苍术酮、苍术素、β-桉叶醇和茅术醇等。苍术素是苍术的主要药效成分之一,也是苍术药材质量控制的重要指标性成分。现代研究表明苍术素具有抗炎、促进胃排空、抗肿瘤、正性肌力、抗菌、保肝、心脏保护、抗氧化等多种药理活性。其抗炎作用广泛,对于肠道炎症、关节炎、气道炎症、肺炎等均有治疗作用,可改善胃肠功能以健脾,抑制胆管癌、肝癌、乳腺癌、肺癌细胞增殖,抑菌作用显著,保肝作用可能与其抗氧化和抗炎活性有关,对于心脏和神经系统也具有保护作用。因此,苍术素药理作用广泛,具有较大的开发应用潜力,随着对其进一步深入研究,越来越多的药理作用机制将会被阐明,对于苍术素的开发利用具有重要促进作用。通过对苍术素的药理作用及机制进行归纳总结,以期为其临床应用及新药开发提供参考。

, authors=杨萍, 李喜香, 宋薇, 王雪梅, authorsList=杨萍, 李喜香, 宋薇, 王雪梅, authorCompany=null, correspAuthors=李喜香, authorNote=

杨萍(1989-),女,甘肃白银人,主管中药师,硕士,研究方向:中药复方及配伍药效机制。

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李喜香(1968-),女,甘肃天水人,主任中药师,硕士研究生导师,研究方向:中药制剂二次开发及中药新剂型。E-mail:。
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杨萍(1989-),女,甘肃白银人,主管中药师,硕士,研究方向:中药复方及配伍药效机制。

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杨萍(1989-),女,甘肃白银人,主管中药师,硕士,研究方向:中药复方及配伍药效机制。

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药理作用剂量实验对象作用机制文献
抗炎50 μmol/LHCT116细胞抑制炎症因子表达及炎症相关信号通路[7-8,10-11,14,17,19-21]
40 mg/kg小鼠
20、40 μmol/LRAW264.7细胞
20 mg/kg小鼠
14 mg/kg小鼠
10 mg/kg大鼠
10、50、100 mg/kg人OA软骨细胞
20、40 mg/kg小鼠
40、80 mg/kg小鼠
100 μmol/LA549细胞
30、90 mg/kg小鼠
10、20、50、100、200 μmol/LNIH3T3细胞
促进胃排空1、10、50 μmol/LHGSMC细胞激活GHSR促进胃排空,提高小肠推进比,调节胃肠动力起搏细胞表达改善胃肠运动[23-25]
0.1、1、10 mg/kg小鼠
0.1~0.3 mg/kg大鼠
1.5、3、6 g/kg大鼠
抗肿瘤50、250、500 μmol/LCL-6细胞调节肿瘤细胞中凋亡及自噬相关蛋白表达,抑制肿瘤细胞增殖、迁移和侵袭,调节细胞周期,诱导细胞凋亡及自噬[28-30,32,36-38]
1.95~250 μg/mLHuCCT-1细胞
20、40、80、160、320、640、1280 μmol/LHuCCT1细胞
5、10、20 μmol/LHuh7,Hccm细胞
20、40、60、80、100 μmol/LA549细胞
10、20、40 μmol/LHCC827细胞
10、20、40、80 mg/LA549细胞
正性肌力作用3 mg/kg大鼠作用于心肌中ghrelin受体,增强SERCA2a活性及肌浆网Ca2+含量促进SR Ca2+瞬时振幅[40-41]
0.1、1、5、10 μmol/L大鼠
3 mg/kg大鼠
0.1、1、10 μmol/L大鼠左心室肌细胞
抗菌30、60 mg/kg小鼠通过上调Nrf2通路和抑制NLRP3炎性体激活阻断细菌生物膜形成及在宿主细胞中复制[43]
4、8 μg/mL小鼠巨噬细胞样细胞系J774A.1
保肝20、40、80 mg/kg小鼠通过调控nrf2介导的铁下垂抑制肝脏中炎症因子表达,调节血清氧化酶含量,减少肝脏氧化损伤,改善肝脏病理性损害[46-47]
10、20、40 μmol/LHepG2细胞
40、80 mg/kg小鼠
10~40 μmol/LHepG2细胞
对心脏的保护作用1000 mg/kg小鼠激活GHSR-Sirt1通路调节SIRT1、IκB、p53蛋白表达,拮抗AngⅡ诱导的房颤易感性增强,保护心肌细胞及肌纤维[49-50]
1 mg/kg小鼠
抗氧化20、40、80 μmol/L人足细胞调控CAT、ROS、SOD等氧化酶的水平,减少细胞氧化应激损伤[52-53]
20、40、80 μmol/L大鼠肾小球足细胞
其他100 μg/mL星形胶质细胞增加嗅觉中NGF的表达来促进嗅觉神经元的再生;抑制脂肪酶生成;激活TRPA1通道产生镇痛作用[54-56]
250、500 mg/kg小鼠
5 μmol/LHEK293细胞
5 mg/kg大鼠
), ArticleFig(id=1322926029756571933, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322926012182438090, language=CN, label=表1, caption=

苍术素的药理作用及机制

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药理作用剂量实验对象作用机制文献
抗炎50 μmol/LHCT116细胞抑制炎症因子表达及炎症相关信号通路[7-8,10-11,14,17,19-21]
40 mg/kg小鼠
20、40 μmol/LRAW264.7细胞
20 mg/kg小鼠
14 mg/kg小鼠
10 mg/kg大鼠
10、50、100 mg/kg人OA软骨细胞
20、40 mg/kg小鼠
40、80 mg/kg小鼠
100 μmol/LA549细胞
30、90 mg/kg小鼠
10、20、50、100、200 μmol/LNIH3T3细胞
促进胃排空1、10、50 μmol/LHGSMC细胞激活GHSR促进胃排空,提高小肠推进比,调节胃肠动力起搏细胞表达改善胃肠运动[23-25]
0.1、1、10 mg/kg小鼠
0.1~0.3 mg/kg大鼠
1.5、3、6 g/kg大鼠
抗肿瘤50、250、500 μmol/LCL-6细胞调节肿瘤细胞中凋亡及自噬相关蛋白表达,抑制肿瘤细胞增殖、迁移和侵袭,调节细胞周期,诱导细胞凋亡及自噬[28-30,32,36-38]
1.95~250 μg/mLHuCCT-1细胞
20、40、80、160、320、640、1280 μmol/LHuCCT1细胞
5、10、20 μmol/LHuh7,Hccm细胞
20、40、60、80、100 μmol/LA549细胞
10、20、40 μmol/LHCC827细胞
10、20、40、80 mg/LA549细胞
正性肌力作用3 mg/kg大鼠作用于心肌中ghrelin受体,增强SERCA2a活性及肌浆网Ca2+含量促进SR Ca2+瞬时振幅[40-41]
0.1、1、5、10 μmol/L大鼠
3 mg/kg大鼠
0.1、1、10 μmol/L大鼠左心室肌细胞
抗菌30、60 mg/kg小鼠通过上调Nrf2通路和抑制NLRP3炎性体激活阻断细菌生物膜形成及在宿主细胞中复制[43]
4、8 μg/mL小鼠巨噬细胞样细胞系J774A.1
保肝20、40、80 mg/kg小鼠通过调控nrf2介导的铁下垂抑制肝脏中炎症因子表达,调节血清氧化酶含量,减少肝脏氧化损伤,改善肝脏病理性损害[46-47]
10、20、40 μmol/LHepG2细胞
40、80 mg/kg小鼠
10~40 μmol/LHepG2细胞
对心脏的保护作用1000 mg/kg小鼠激活GHSR-Sirt1通路调节SIRT1、IκB、p53蛋白表达,拮抗AngⅡ诱导的房颤易感性增强,保护心肌细胞及肌纤维[49-50]
1 mg/kg小鼠
抗氧化20、40、80 μmol/L人足细胞调控CAT、ROS、SOD等氧化酶的水平,减少细胞氧化应激损伤[52-53]
20、40、80 μmol/L大鼠肾小球足细胞
其他100 μg/mL星形胶质细胞增加嗅觉中NGF的表达来促进嗅觉神经元的再生;抑制脂肪酶生成;激活TRPA1通道产生镇痛作用[54-56]
250、500 mg/kg小鼠
5 μmol/LHEK293细胞
5 mg/kg大鼠
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苍术素药理作用及机制的研究进展
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杨萍 , 李喜香 , 宋薇 , 王雪梅
中华中医药学刊 | 国家项目点击 2025,43(7): 114-120
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中华中医药学刊 |国家项目点击 2025 , 43 (7) : 114 -120
苍术素药理作用及机制的研究进展
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杨萍, 李喜香 , 宋薇, 王雪梅
作者信息
  • 甘肃省中医院,甘肃 兰州 730050
通讯作者:
李喜香(1968-),女,甘肃天水人,主任中药师,硕士研究生导师,研究方向:中药制剂二次开发及中药新剂型。E-mail:。
作者简介:

杨萍(1989-),女,甘肃白银人,主管中药师,硕士,研究方向:中药复方及配伍药效机制。

Research Progress on Pharmacological Action and Mechanism of Cangzhu(Atractylodis Rhizoma)
Ping YANG, Xixiang LI , Wei SONG, Xuemei WANG
Affiliations
  • Gansu Provincial Hospital of Traditional Chinese Medicine,Lanzhou 730050,Gansu,China
出版时间: 2025-07-10 doi: 10.13193/j.issn.1673-7717.2025.07.025
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苍术为中医临床常用的大宗中药,药用历史悠久,具有燥湿健脾、祛风散寒、明目的功效,在胃肠道疾病、风湿性疾病中应用广泛,临床疗效显著。主要活性成分为挥发油类,包括苍术酮、苍术素、β-桉叶醇和茅术醇等。苍术素是苍术的主要药效成分之一,也是苍术药材质量控制的重要指标性成分。现代研究表明苍术素具有抗炎、促进胃排空、抗肿瘤、正性肌力、抗菌、保肝、心脏保护、抗氧化等多种药理活性。其抗炎作用广泛,对于肠道炎症、关节炎、气道炎症、肺炎等均有治疗作用,可改善胃肠功能以健脾,抑制胆管癌、肝癌、乳腺癌、肺癌细胞增殖,抑菌作用显著,保肝作用可能与其抗氧化和抗炎活性有关,对于心脏和神经系统也具有保护作用。因此,苍术素药理作用广泛,具有较大的开发应用潜力,随着对其进一步深入研究,越来越多的药理作用机制将会被阐明,对于苍术素的开发利用具有重要促进作用。通过对苍术素的药理作用及机制进行归纳总结,以期为其临床应用及新药开发提供参考。

苍术素  /  抗炎  /  胃排空  /  抗肿瘤  /  正性肌力  /  抗菌  /  保肝

Cangzhu(Atractylodis Rhizoma)is a major traditional Chinese medicine commonly used in TCM clinical practice and has a long history of medicinal use. It has the effect of drying dampness and strengthening spleen,dispelling wind and dispelling cold,and brightening eyes. It is widely used in gastrointestinal diseases and rheumatic diseases,the clinical effect is remarkable. The main active ingredients are volatile oils,including atractyloketone,atractylotin,β-phylloalcohol and citronol. Atractylotin is one of the main efficacy components of Cangzhu(Atractylodis Rhizoma). It is also an important index component for quality control of Cangzhu(Atractylodis Rhizoma). Modern pharmacological studies have shown that atractylotin has anti-inflammatory,gastric emptying,anti-tumor,positive muscle strength,antibacterial,liver protection,heart protection,antioxidant activities. It has a wide range of anti-inflammatory effects and therapeutic effects on intestinal inflammation,arthritis,airway inflammation,pneumonia,etc. It can improve gastrointestinal function to strengthen spleen,inhibit the proliferation of bile duct cancer,liver cancer,breast cancer and lung cancer cells,and has significant antibacterial effect. The liver protection effect may be related to its antioxidant and anti-inflammatory activities,and it also has protective effects on the heart and nervous system. Atractylotin has a wide range of pharmacological effects and great potential for development and application. With further research,more and more pharmacological mechanisms will be elucidated,which will play an important role in promoting the development and utilization of atractylotin. The pharmacological action and mechanism of atractylotin were summarized in order to provide reference for its clinical application and new drug development.

atractylotin  /  anti-inflammatory  /  gastric emptying  /  anti-tumor  /  positive inotropic  /  antibacterial  /  liver protection
杨萍, 李喜香, 宋薇, 王雪梅. 苍术素药理作用及机制的研究进展. 中华中医药学刊, 2025 , 43 (7) : 114 -120 . DOI: 10.13193/j.issn.1673-7717.2025.07.025
Ping YANG, Xixiang LI, Wei SONG, Xuemei WANG. Research Progress on Pharmacological Action and Mechanism of Cangzhu(Atractylodis Rhizoma)[J]. Chinese Archives of Traditional Chinese Medicine, 2025 , 43 (7) : 114 -120 . DOI: 10.13193/j.issn.1673-7717.2025.07.025
苍术为菊科植物茅苍术Atractylodes lancea(Thunb.)DC.或北苍术Atractylodes chinensis(DC.)Koidz.的干燥根茎,性温,味辛、苦,归脾、胃、肝经,临床主要用于湿阻中焦,脘腹胀满,泄泻,水肿,脚气痿躄,风湿痹痛,风寒感冒,夜盲,眼目昏涩等症[1]。苍术主要含有挥发油,含量5%~9%[2],挥发油化学成分复杂,以烯烃、醇类、酯类、酮类、酸类化合物为其主要类型,其中烯烃类化合物为其主要成分,包括苍术素、苍术酮、苍术醇、β-桉叶醇、茅术醇等[3]。苍术素为无色针晶,是一种炔类化合物,现代药理研究表明具有降血糖、利尿、促进胃排空、抗炎、抗肿瘤等作用[4],化学结构见图1。因此,通过总结苍术素的药理作用及机制,为其药物开发及临床应用提供理论依据。
炎症是各种慢性疾病进展的主要因素,包括糖尿病、癌症、心血管疾病、眼疾、关节炎、肥胖、自身免疫性疾病和炎症性肠病等[5]。苍术素抗炎作用广泛,对于多种炎症均有治疗作用,如肠道炎症、关节炎、气道炎症、肺炎等。
肠道炎症疾病如克罗恩病、溃疡性结肠炎和坏死性肠炎等患病人群日益增多,可造成肠道屏障受损,导致细菌易位引起全身炎症,严重者还会导致脓毒症[6]。HEO G等[7]发现苍术素50μmol/L显著抑制结肠上皮细胞HCT116中肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)诱导的核因子-κB p65(nuclear factor-κB p65,NF-κB p65)磷酸化,通过对接模拟分析、荧光素酶检测及体内作用研究,发现苍术素对过氧化物酶体增殖物激活受体α(peroxisome proliferatoractivated receptor-α,PPARα)具有亲和力,苍术素40 mg/kg可减轻右旋糖酐硫酸钠(dextran sulfate sodium,DSS)诱导的结肠炎模型小鼠结肠炎症状,提高小鼠存活率,表明苍术素可通过诱导PPARα依赖性途径治疗结肠炎。QU L等[8]发现苍术素20 mg/kg可显著改善DSS诱导的溃疡性结肠炎的进展,减轻结肠损伤,减少结肠杯状细胞损失,增加紧密连接蛋白(zonula occludens-1,ZO-1)、闭锁蛋白(occludin,OCLN)、黏蛋白2(mucin-2,MUC2)表达,抑制结肠组织巨噬细胞活化,下调炎症因子表达,保护肠道屏障,减少有害细菌丰度并增加有益细菌丰度,从而改善整体肠道微生物群,并可抑制乳酸产生、磷酸甘油醛脱氢酶(glyceraldehyde phosphate dehydrogenase,GAPDH)活性和GAPDH蛋白丙二酰化,进而抑制TNF-α表达,在体内和体外抑制RAW264.7细胞中炎症丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)通路的激活,表明苍术素通过减轻肠道菌群失调并通过MAPK途径抑制炎症反应来减轻DSS诱发的结肠炎。ISHIGURO K等[9]发现苍术素抑制4-Chloro-7-硝基-2,1,3-苯并恶二唑(NBD-Cl)诱导的结肠炎模型中活化的成纤维细胞中白细胞介素(interleukin,IL)-6生成,在TNF-α刺激下,苍术素诱导组蛋白H3在赖氨酸残基9处发生三甲基化,从而抑制NF-κB与基因组DNA上IL-6启动子之间的结合,抑制赖氨酸特异性去甲基化酶4A(recombinant lysine specific demethylase 4A,KDM4A)但不抑制KDM6A活性,用KDM4A抑制剂ML324对IL-6产生和结肠炎诱导表现出类似的作用,因此,苍术素可能通过抑制KDM4A活性来抑制IL-6产生和减弱结肠炎诱发。董雪等[10]研究发现苍术素14 mg/kg能够改善溃疡性结肠炎模型小鼠的结肠缩短、体质量下降及疾病活动指数评分升高等指标,减轻结肠损坏程度,对DSS诱导的溃疡性结肠炎具有一定防治效果。苍术素10 mg/kg可减少便秘型(CP)和腹泻型(DP)大鼠血浆中促炎细胞因子TNF-α、IL-1β和IL-6表达,抑制空肠段炎症介质诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)和NF-κB表达,表明苍术素对CP和DP大鼠空肠节段的收缩力分别具有刺激作用和抑制作用,表现出收缩状态依赖性调节,显著上调CP大鼠和下调DP大鼠空肠段20 kDa肌球蛋白轻链磷酸化水平、肌球蛋白轻链激酶(myosin light chain kinase,MLCK)蛋白含量和MLCK mRNA表达,表明苍术素可能具有改善便秘和腹泻大鼠肠道炎症的作用[11]。综上所述,苍术素可能通过PPARα及MAPK途径抑制肠道组织巨噬细胞活化,下调炎症因子表达,改善肠道损坏程度,减弱肠道炎症诱发。
关节炎是以滑膜炎症和进行性关节破坏为特征的一种慢性疾病,会造成不可逆转的关节破坏[12]。CHUANG CH等[13]通过建立胶原诱导性关节炎小鼠模型,发现苍术素显著减轻爪肿胀、关节炎评分和关节组织病理变化,降低Ⅱ型胶原诱导的T细胞增殖及脾脏中Th1和Th17丰度,下调脾脏树突状细胞(DC)CD40、CD80和CD86表达,抑制脂多糖(Lipopolysaccharides,LPS)孵育的DC中促炎细胞因子分泌、共刺激分子表达及p38 MAPK、细胞外信号调节激酶(extracellular signal regulated kinase,ERK)和NF-κB p65信号通路,和增殖及细胞因子γ-干扰素(interferonγ,IFN-γ)和IL-17A分泌T细胞减少,表明苍术素可抑制树突状细胞成熟并改善胶原诱导的关节炎。邱伟建等[14]发现苍术素(10、50、100 mg/kg)显著降低IL-1β诱导的人OA软骨细胞中基质金属蛋白酶1(matrix metalloproteinase 1,MMP1)、MMP13、环氧合酶-2(cyclooxygenase-2,COX-2)、NO表达,通过抑制IL-1β介导的NF-κB活化以缓解软骨细胞炎性反应,并通过激活肝X受体α(recombinant liver X receptor alpha,LXRα)的活性以抑制IL-1β介导的软骨细胞炎性反应,表明苍术素在人OA软骨细胞中有抗炎活性作用。综上所述,苍术素可改善关节软骨炎性反应,可能通过抑制p38 MAPK、ERK和NF-κB p65信号通路缓解软骨细胞炎性反应,从而发挥抗关节炎作用。
气道炎症通常由病原体或接触毒素、污染物、刺激物和过敏原引起,严重者可能危及生命[15]。DONG Y等[16]发现苍术素抑制LPS诱导的人气道上皮细胞(16HBE)中IL-6、IL-8和MUC5AC mRNA表达,下调Ⅰ型胶原(recombinant collagen typeⅠ,Col-Ⅰ)和纤维连接蛋白(fibronectin,FN)水平,抑制NF-κB通路激活,表明苍术素通过抑制NFκB通路减轻脂多糖诱导的气道炎症中MUC5AC和细胞外基质表达;苍术素还可抑制小鼠卵清蛋白诱导的气道炎症和NF-κB通路,表明苍术素具有改善气道炎症作用。LIN Y C等[17]发现苍术素20、40 mg/kg减轻卵清蛋白(OVA)诱导的小鼠变应性气道炎症,下调肺组织中辅助T2(Th2)相关细胞因子IL-4、IL-5、IL-13水平,降低OVA特异性IgG1和IgE的产生,将OVA刺激小鼠的DC分离后与OVA特异性T细胞共培养,发现脾细胞增殖减少,表明苍术素可能通过调节DC的成熟来改善OVA诱导的过敏性哮喘模型中的气道高反应性(AHR)和抗原特异性Th2细胞炎症。综上,苍术素可能通过抑制NF-κB通路激活,下调气道上皮细胞中炎症因子及黏蛋白表达,调节脾树突状细胞成熟,从而改善气道炎症。
肺炎是影响肺泡、呼吸细支气管和肺间质的急性炎症性疾病,为传播最广泛的传染病之一,目前主要采用抗生素减少并发症的发生[18]。TANG F等[19]发现苍术素(40或80 mg/kg)显著减轻LPS诱导的急性肺损伤模型小鼠肺组织病理学变化,减少髓过氧化物酶(myeloperoxidase,MPO)活性、肺湿干重比、蛋白质渗漏和炎症细胞浸润,抑制支气管肺泡灌洗液中TNF-α、IL-6、IL-1β和单核细胞趋化蛋白(monocyte chemotactic protein-1,MCP-1)分泌,表明苍术素可能是通过抑制核苷酸结合域(NOD-)样受体蛋白3(NLRP3)炎性体和Toll样受体4(Toll like receptor 4,TLR4)的激活减轻LPS引起的肺损伤而发挥抗炎作用。CHANG K W 等[20]发现苍术素100μmol/L可减弱肺泡上皮细胞A549中转化生长因子-β1(transforming growth factor-β1,TGF-β1)诱导的2型肺上皮细胞上皮间质转化(epithelial-mesenchymal transition,EMT)和博莱霉素诱导的小鼠肺纤维化,减少胶原蛋白沉积和降低E-钙黏蛋白表达,可能通过Smad和非Smad途径下调转录因子Snail和Slug的表达,从而影响TGF-β1介导的EMT。WU Z H等[21]发现苍术素30、90 mg/kg改善博来霉素(BLM)诱导的肺纤维化模型小鼠的呼吸功能,减轻肺部炎症,降低肺组织中纤维化标志物a-SMA、纤连蛋白和col1A1表达及羟脯氨酸含量,抑制纤维形成,还可减轻纤维化形成后期肺部炎症反应,下调TGF-β1诱导的小鼠胚胎成纤维细胞NIH3T3中Smad 2和Smad 3磷酸化水平,抑制Smad 2/3信号传导激活,表明苍术素可能通过抑制Smad 2/3信号通路的活性来抑制TGF-β1诱导的成纤维细胞分化。综上,苍术素可能是通过介导NLRP3炎性体和TLR4的激活及Smad和非Smad途径下调肺组织中炎症因子表达,减轻肺损伤及肺部炎症。
因此,苍术素在多种炎症性疾病中均表现出抗炎作用,可能通过抑制炎症因子表达及炎症相关信号通路减少组织炎性细胞浸润,具体机制见插页ⅩⅩⅩⅨ图2。
苍术治疗脾胃疾病历史悠久,疗效显著,历代医籍中记录了诸多以苍术入药治疗脾胃的方剂,如平胃散补脾胃泻阴火,升阳汤、完带汤等均为燥湿健脾、和胃行气的经典名方[22],现代药理研究表明苍术素在调节脾胃疾病方面发挥着重要作用。BAI Y等[23]发现苍术素通过激活生长激素促分泌素受体(growth hormone secretagogue receptor,GHSR)增加人胃平滑肌细胞HGSMC中的Ca2+并增强肌球蛋白轻链(myosin light chain,MLC)磷酸化,在体内可通过激活GHSR促进小鼠胃排空并诱导胃窦MLC磷酸化,表明苍术素是一种潜在的适合治疗以胃排空延迟为特征的疾病的药物,例如功能性消化不良。NAKAI Y等[24]发现0.1~0.3 mg/kg苍术素以剂量依赖性方式改善NG-硝基-l-精氨酸引起的大鼠胃排空延迟。苍术素能减少大鼠胃内残留率,提高小肠推进比,增强机体整体及胃黏膜局部的防御机制,改善脾虚湿阻证大鼠胃黏膜的病理损伤,修复脾虚模型大鼠胃黏膜组织细胞的超微结构,上调胃黏膜三叶因子1(TFF1)及Cajal间质细胞c-kit表达,表明苍术素对胃肠动力起搏细胞ICC表达的调节可能是调控胃肠运动治疗脾虚湿阻证的重要机制[25]。综上,苍术素可能通过激活GHSR促进胃排空,提高小肠推进比,调节胃肠动力起搏细胞表达改善胃肠运动。见插页ⅩⅩⅩⅨ图3。
中药及其活性成分在癌症中的应用历史悠久,具有靶点多、不良反应少的优势[26]。研究表明苍术素抗肿瘤作用广泛,对胆管癌、肝癌、乳腺癌、肺癌等均具有治疗作用。
胆管癌是一组异质性胆管肿瘤,是继肝细胞癌之后第二常见的肝癌,其发病率呈整体上升趋势[27]。MATHEMA V B等[28]发现苍术素对胆管癌相关细胞系CL-6表现出选择性细胞毒性,抑制CL-6细胞的集落形成能力并降低伤口愈合电位,减少血红素氧合酶-1(heme oxygenase-1,HO-1)的产生,抑制STAT1/3蛋白磷酸化,下调NF-κB p50、NF-κB p52、NF-κB p65蛋白表达,且呈剂量依赖性和时间依赖性,表明苍术素对CL-6细胞具有明显的细胞毒作用,可能与其抑制HO-1生成、STAT1/3磷酸化及关键NF-κB蛋白表达有关。VANAROJ P等[29]发现苍术素对胆管上皮癌细胞HuCCT-1生长有中度抑制作用,不同浓度苍术素处理HuCC-T1细胞后,Notch1基因表达水平均显著下调,其基因表达的程度和变化与蛋白表达有良好的相关性,表明苍术素可能是通过抑制Notch1信号通路来抑制胆管癌细胞增殖。苍术素以时间和剂量依赖的方式诱导HuCCT1细胞自噬,以浓度依赖的方式诱导其迁移和侵袭,SB202190(自噬诱导剂)和3-MA(自噬抑制剂)分别显著提高和降低苍术素诱导的自噬率,苍术素作用24 h可抑制磷酯酰肌醇3-激酶(phosphatidylinositol 3-kinase,PI3K)、蛋白激酶B(protein kinase B,AKT)、雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)、p38MAPK磷酸化,增加自噬标记蛋白(Beclin-1)表达和LC3转化,表明苍术素通过调节PI3K/AKT/mTOR和p38MAPK信号通路抑制胆管癌细胞增殖,并诱导其自噬[30]。综上,苍术素可能通过调节HO-1、磷酸化STAT1/3及NF-κB蛋白表达,调控Notch1及PI3K/AKT/mTOR和p38MAPK信号通路抑制胆管癌细胞增殖,并诱导细胞自噬。
肝癌是全球最常见的癌症死亡原因,其预后较差,无论是目前的消融疗法还是化疗都不能明显有效地改善症状,因此有必要进一步寻找更好的治疗方法[31]。HE Y等[32]发现苍术素能抑制人肝癌细胞株(Huh7和Hccm)的增殖、迁移和侵袭,调节细胞周期,诱导细胞凋亡和G1期细胞周期阻滞,显著诱导细胞内活性氧(reactive oxygen species,ROS)水平升高,上调酰基辅酶A合成酶长链家族成员4(acyl-CoA synthetase long-chain family member 4,ACSL4)、转铁蛋白受体1(recombinant transferrin receptor,TFR1)表达,下调谷胱甘肽过氧化酶4(recombinant glutathione peroxidase 4,GPX4)、轻肽铁蛋白(ferritin light polypeptide,FTL)表达,从而诱导肝癌细胞中的铁死亡。综上,苍术素可抑制肝癌细胞增殖、迁移和侵袭,调节细胞周期,诱导细胞凋亡,但其抗肝癌作用文献报道相对较少,具体作用机制仍需进一步深入研究。
乳腺癌是女性最常见的癌症,也是全世界第2种经常发生的新诊断癌症[33]。LI Z等[34]发现苍术素对人乳腺癌细胞MCF-7具有浓度依赖性毒性,增加乳过氧化物酶(lactoperoxidase,LPO)、ROS,降低超氧化物歧化酶(superoxide dismutase,SOD)、过氧化氢酶(catalase,CAT)和谷胱甘肽过氧化物酶(glutathione peroxidase,GPX4)活性,降低B淋巴细胞瘤-2(B-cell lymphoma-2,Bcl-2)表达,同时激活p53、Bcl-2相关X蛋白(Bcl-2 associated X protein,Bax)、裂解的半胱氨酸天冬氨酸蛋白酶-3(cystein-asparate protease-3,Caspase-3)、Caspase-8和Caspase-9表达,阻断P13K/AKT/mTOR信号通路,增加自噬相关蛋白微管相关蛋白轻链3Ⅰ(microtubule-associated protein light chain 3Ⅰ,LC3Ⅰ)向脂化形式LC3Ⅱ转化,增加Beclin-1表达,下调MCF-7细胞中p62表达,表明苍术素通过改变凋亡和自噬相关的生物标志物诱导MCF-7细胞凋亡和自噬。综上,苍术素可通过抑制P13K/AKT/mTOR信号通路调节乳腺癌细胞中凋亡及自噬相关蛋白表达,发挥抗乳腺癌作用。但有关其抗乳腺癌作用国内外文献报道相对较少,需在今后加强该方向的研究。
肺癌发病率逐年上升,病死率高,是我国公共卫生的重要问题,也是社会的一大负担[35]。ZHANG T等[36]研究表明苍术素通过诱导细胞内ROS积累及调节MAPK、转录激活因子3(signal transducer and activator of transcription 3,STAT3)及NF-κB信号通路诱导人非小细胞肺癌(NSCLC)细胞A549凋亡,并诱导AKT信号通路调节的细胞周期G2/M 期阻滞和Wnt信号通路调节的细胞迁移,且苍术素对A549细胞凋亡的影响与线粒体膜电位的变化呈负相关。朱亚兰等[37]发现10、20、40μmol/L的苍术素可显著抑制NSCLC细胞HCC827的迁移与侵袭,且呈药物浓度依赖性,上调E-钙黏蛋白(E-cadherin)表达,下调N-cadherin、Snail1蛋白表达,抑制酪氨酸激酶2(Janus kinase 2,JAK2)、STAT3蛋白磷酸化水平,表明苍术素通过抑制JAK2/STAT3通路抑制HCC827细胞增殖、迁移、侵袭和细胞上皮间质转化。张美楠等[38]采用苍术素处理A549细胞,发现浓度为40 mg/L时,细胞增殖率及侵袭和迁移数下降,CyclinD1及MMP-9表达显著下调,细胞凋亡率及Bax表达显著增加,STING、cGAS表达显著上调,表明苍术素通过激活cGAS-STING信号通路抑制肺癌细胞恶性生物学行为,进而发挥抗肿瘤免疫作用。综上发现苍术素可通过调控多条信号通路抗肺癌,包括MAPK、STAT3、NF-κB、AKT、Wnt、JAK2/STAT3及cGAS-STING通路等,诱导肺癌细胞凋亡,调节细胞周期阻滞,抑制其增殖、迁移和侵袭。见插页ⅩⅩⅩⅨ图4。
正性肌力药物在心力衰竭治疗中占有很重要的地位,目前有关正性肌力中药的报道很多,但作用机制尚未明确,因此需要进一步深入研究[39]。GAO L等[40]发现苍术素3 mg/kg显著增加左心室每搏功、心输出量、每搏输出量、心率、射血分数、收缩末压、左心室压力升降峰值速率、收缩末期压力-容积关系的斜率及收缩末期容积和舒张末期容积的减少,降低舒张压和动脉弹性;苍术素0.1、1、10μmol/L增加离体大鼠心脏左室压,Ghrelin受体无偏拮抗剂JMV-2959(1μmol/L)可阻断其作用;苍术素5μmol/L通过增强SERCA2a活性、肌浆网Ca2+含量及受磷蛋白16-丝氨酸的磷酸化增加Ca2+瞬时振幅,表明苍术素通过增强SERCA2a活性而具有正性肌力作用,可能是通过作用于心肌中的ghrelin受体介导的。苍术素3 mg/kg显著增加心率、心排血量和每搏功,降低舒张压,0.1、1、10 μmol/L显著增加左心室展开压,且呈浓度依赖性,10μmol/L显著增加促进肌浆网SERCA2a介导的SR Ca2+瞬时振幅,PKA抑制剂H89可阻断SR Ca2+瞬变幅度的增强,从而阻断苍术素的正性肌力作用,表明苍术素在体内外均对大鼠心脏具有正性肌力作用,降低舒张压,可能是通过PKA-SERCA2a信号通路介导的[41]。综上,苍术素可能通过作用于心肌中ghrelin受体,增强SERCA2a活性及肌浆网Ca2+含量促进SR Ca2+瞬时振幅,进而发挥正性肌力作用。见插页ⅩⅩⅩⅨ图5。
中药化学成分多样,具有较好地抑菌活性,但其作用机制可能并不单一,明确中药发挥抗菌活性的作用机制,能够为临床治疗感染性疾病的用药提供更广阔的选择空间,更好地帮助临床用药[42]。XU L等[43]发现苍术素通过减少李斯特菌溶血素O(LLO)的产生和溶血活性来阻碍LLO功能,消除LLO孔的形成,抑制其生物膜的形成及在宿主细胞中的复制,显著抑制其病理生理过程,有效保护单核细胞增生李斯特菌引起的组织损伤免受氧化应激和炎症损伤,增强核因子E2相关因子2(nuclear factor erythroid 2-related factor 2,Nrf2)激活,抑制NLRP3介导的Caspase-1激活和IL-1β表达,表明苍术素具有通过上调Nrf2通路和抑制小鼠NLRP3炎性体激活来对抗单核细胞增生李斯特菌感染的抗炎潜力。李建航等[44]研究表明苍术素对耐药性菌株有显著地抑制作用,可有效消除碳青霉烯耐药大肠埃希氏菌菌株的耐药质粒,最小抑菌浓度为25 mg/mL。综上发现苍术素可通过上调Nrf2通路和抑制NLRP3炎性体激活阻断细菌生物膜形成及在宿主细胞中复制发挥抗菌作用,但其对除上述病原菌以外的耐药菌有无作用及其抗菌机制还有待深入研究。见插页ⅩⅩⅩⅨ图6。
肝脏疾病是世界上导致死亡的主要原因之一,尽管现代药物研究取得了巨大进步,但仍然迫切需要有效且安全的保肝药物,天然产物无疑是先导药物的宝贵来源[45]。YE Q等[46]发现苍术素可通过降低Fe2+浓度、ROS水平、丙二醛含量和谷胱甘肽含量,抑制肝细胞铁下垂来减轻高脂肪饮食(HFD)诱导的小鼠非酒精性脂肪肝(NAFLD),对肝细胞活力的保护作用被一种特异性的铁凋亡抑制剂(铁抑素-1)阻断,促进核因子红系2相关因子2(NFE2L2/NRF2)易位,从而增加GPX4、铁蛋白重链1(FTH1)和溶质载体家族7成员11(SLC7A11)的表达,表明苍术素通过调节nrf2介导的铁下垂来缓解NAFLD。LYU Z等[47]发现苍术素可降低急性肝衰竭(ALF)高致死率,降低血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、单核细胞趋化蛋白(monocyte chemotactic protein-1,MCP-1)、IL-1β、IL-6和TNF-α水平,改善ALF的病理性肝损害。综上,苍术素可通过调控Nrf2介导的铁下垂抑制肝脏中炎症因子表达,调节血清氧化酶含量,减少肝脏氧化损伤,从而改善肝脏病理性损害。然临床肝损伤形式多样,其病因复杂,关于苍术素在其他类型肝损伤中的作用仍需深入探讨。见插页ⅩⅩⅩⅨ图7。
心血管疾病是现代社会发病率和病死率居高不下的主要原因,寻求具有更多预防或治疗价值的药物是当前研究的重点,中药作为天然药物分子的巨大宝库,在临床防治心血管疾病方面有着悠久的历史[48]。ZHAN Y等[49]发现1000 mg/kg苍术可减轻小鼠心房间质纤维化及持续输注血管紧张素Ⅱ(AngⅡ)诱导的促纤维化和促炎信号,在体内试验和离体灌注心脏中,苍术减弱AngⅡ诱导的房颤易感性增强,促进AngⅡ诱导的沉默调节蛋白1(Sirtuin 1,Sirt1)易位至细胞核,抑制IκB磷酸化、p53过度表达及细胞凋亡,对AngⅡ的所有拮抗作用均因GHSR抑制剂的联合治疗而减弱,表明苍术可能通过增强GHSR-Sirt1途径预防心房纤维化并减弱AngⅡ诱发的房颤的易感性增强,苍术素其抗纤维化活性与苍术相当。FUJITSUKA N等[50]发现苍术素减少大脑中小胶质细胞的激活,延长klotho缺陷的SAMP8和老年ICR小鼠的生存时间,在表达胃饥饿素(Ghrelin)受体1a的细胞和人脐静脉内皮细胞中,经过ghrelin和ghrelin增强剂处理后,观察到通过cAMPCREB途径提高的Sirt1活性和蛋白表达,表明苍术素增加衰老小鼠模型中下丘脑Sirt1活性和心脏Sirt1蛋白表达,改善心包炎、心肌钙化及心肌和肌纤维萎缩。综上苍术素可能通过激活GHSR-Sirt1通路调节Sirt1、IκB、p53蛋白表达,拮抗AngⅡ诱导的房颤易感性增强,保护心肌细胞及肌纤维。见插页ⅩⅩⅩⅨ图8。
细胞的化学反应会导致自由基的产生,自由基与脂质、蛋白质和DNA等有机底物发生反应,通过氧化自由基对这些分子造成损害,扰乱它们的正常功能,因此可能导致多种疾病[51]。CHEN L等[52]研究表明苍术素抑制足细胞过度运动,并上调裂隙隔膜蛋白podocin和nephrin,以及细胞骨架蛋白CD2相关蛋白(CD2AP)、α-Actinin-4和突触足蛋白的表达,这些蛋白与CAT和SOD 1表达上调所证明的抗氧化活性一致,以及减少ROS的产生。陈利[53]发现苍术素20、40和80 μmol/L减少果糖诱导大鼠肾小球足细胞ROS水平并抑制其氧化应激反应,40、80μmol/L上调SOD1和CAT水平,下调TRPC6和p-CaMK4并恢复Synaptopodin蛋白表达,表明苍术素可能通过抗氧化调节TRPC6-Ca2+-CaMK4-Synaptopodin信号抑制果糖诱导的足细胞过度迁移。综上苍术素抗氧化机制可能与调控CAT、ROS、SOD等氧化酶的水平,减少细胞氧化应激损伤有关,但其抗氧化作用仅体现在抑制足细胞过度运动方面,与其他疾病之间的联系研究报道较少,尚需进一步阐释。见插页ⅩL图9。
研究表明苍术素还具有神经保护、抗肥胖、镇痛等药理作用。NODA T等[54]发现苍术素增强小鼠嗅觉标记蛋白、Ki-67和神经生长因子(nerve growth factor,NGF)在嗅觉上皮细胞中的表达,使用大鼠原代培养的星形胶质细胞,发现苍术素可增加NGF的表达,表明苍术素通过增加嗅觉中NGF的表达来促进嗅觉神经元的再生。苍术素对脂肪酶的抑制作用显著,具有抗肥胖作用,其IC50为39.12μmol/L[55]。KANDA H等[56]发现苍术素在表达hTRPA1的HEK293细胞中增加瞬时受体电位锚蛋白-1(TRPA1)单通道活性,在TRPA1基因敲除小鼠的背根神经节神经元中,大量应用苍术素可产生持久的钙反应,且反应完全减弱,表明苍术素是TRPA1通道的独特激动剂,通过长期激活TRPA1通道产生镇痛作用。综上所述,苍术素对神经系统疾病也有治疗作用,还可降脂治疗肥胖,对疼痛刺激等可产生镇痛作用,具有广阔的开发应用前景,但其具体的作用机制尚未完全阐明,需在今后的研究中加强。苍术素的药理作用及机制见表1。
苍术素是中药苍术的主要药效成分,也是苍术质量控制的重要指标性成分,具有广泛的生物活性,对多种疾病均有显著的治疗作用,在食品添加剂、保健品、饲料添加剂、农药杀虫及杀菌剂等行业也有应用。目前,对苍术素的抗炎、促进胃排空、抗肿瘤、正性肌力、抗菌、保肝、心脏保护、抗氧化等药理作用及机制研究较为深入,关于其降血糖、利尿等药理作用文献报道相对较少,还需进一步开展实验研究。
苍术素的稳定性较差,不易保存。在高温及强光下易分解,超临界CO2萃取法可以有效避免苍术素在提取过程中被高温分解,同时以CO2作为萃取剂大大提升了提取物的纯度,是目前提取苍术素的较佳工艺[57]。杨冬丽等[58]采用气相色谱测定颈复康制剂挥发油中苍术素的含量,并对其在不同介质中的稳定性进行考察,结果发现低温有助于保持苍术素的稳定性,且贮存时间不宜过长。谢晓玲等[4]考察苍术素在药材细粉、挥发油、脂溶性膏剂及β-环糊精包合物、β-环糊精混合物中的稳定性,结果发现苍术素在药材及制剂中存在不同程度的光、热不稳定性,药材细粉和挥发油中的苍术素相较于其他存在形式更稳定。杨帆等[59]发现光照条件对苍术中苍术素含量有显著影响,且随着光照时间和强度的增加,呈明显下降趋势,但当光照强度达到1021 Lx以后,光照时长达到4 h以后,苍术素的降解变化不明显。因此,对苍术素进行结构修饰改良以提高其稳定性对于苍术素的药物开发及临床应用具有重要意义。
综合以上苍术素的药理作用及化学性质,对于苍术素的提取纯化和结构修饰改良及药理作用机制的深入研究将会是后续进一步研究的方向,结构修饰改良必需以保证苍术素的药效为前提,以期将苍术素开发为质量稳定、临床疗效显著且具有靶向作用的改良型新药。
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2025年第43卷第7期
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doi: 10.13193/j.issn.1673-7717.2025.07.025
  • 首发时间:2026-10-30
  • 出版时间:2025-07-10
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国家中医药管理局科技司-中央财政转移支付地方项目实施方案-中药创新能力提升项目(甘财社〔2023〕53号)
中央转移支付医疗服务与保障能力提升(中医药事业传承与发展部分)-中医药人才培养重点学科建设项目(甘财社〔2022〕48号)
甘肃省中医药管理局项目(GZKP-2023-11)
兰州市科技计划项目(2022-3-35)
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    甘肃省中医院,甘肃 兰州 730050

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李喜香(1968-),女,甘肃天水人,主任中药师,硕士研究生导师,研究方向:中药制剂二次开发及中药新剂型。E-mail:。
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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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