Article(id=1322923613556454234, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322923490592043032, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2025.05.026, 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=1793339168204, onlineDateStr=2026-10-30, pubDate=1746806400000, pubDateStr=2025-05-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1793339168204, onlineIssueDateStr=2026-10-30, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1793339168204, creator=13701087609, updateTime=1793339168204, updator=13701087609, issue=Issue{id=1322923490592043032, tenantId=1146029695717560320, journalId=1255847919539208197, year='2025', volume='43', issue='5', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1746806400000', pubDateStr='2025-05-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1793339138887, creator='13701087609', updateTime=1793340572227, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1322929502539612595, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322923490592043032, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1322929502539612596, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322923490592043032, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=129, endPage=138, ext={EN=ArticleExt(id=1322923613757780827, articleId=1322923613556454234, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Research Progress on Renshen(Ginseng Radix et Rhizoma)Regulating Immune System Diseases and Quality Marker Prediction Analysis, columnId=1256183361521967297, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Target on National Project, runingTitle=null, highlight=null, articleAbstract=

Renshen(Ginseng Radix et Rhizoma)is the dried root and rhizome of plant Renshen(Panax ginseng C. A. Mey.). The main chemical components include saponins,polysaccharides,polyynols,volatile oils,proteins,peptides,amino acids,etc. In this paper,based on the summary of the chemical composition and pharmacological effects of Renshen(Ginseng Radix et Rhizoma)regulating immune function and the principle of quality marker(Q-Marker),the plant affinity,the effectiveness of chemical components,the specificity and the compatibility of compound formulae were predicted and analyzed. Ginsenosides,polysaccharides,proteins and volatile oils were the Q-Markers of Renshen(Ginseng Radix et Rhizoma)regulating immune function,and ginsenosides Rg1,Re,Rb1,Rg3,Rh1,Rh2,Rd,CK,Ro,Rg5,ginseng D-glucose,galactose,arabinose and ginsekyl can be selected as alternative substances for a single component,which can provide a certain quality control method reference.

, authors=Hui XU1, Jing RAN1, Dan WANG2, Wei ZHANG1, Xueyuan BAI1, authorsList=Hui XU, Jing RAN, Dan WANG, Wei ZHANG, Xueyuan BAI, authorCompany=null, correspAuthors=Wei ZHANG, Xueyuan BAI, 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=1322923614751830882, articleId=1322923613556454234, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=人参调节免疫系统疾病研究进展及质量标志物预测分析, columnId=1256183362172142382, journalTitle=中华中医药学刊, columnName=国家项目点击, runingTitle=null, highlight=null, articleAbstract=

人参为五加科(Araliaceae)植物人参Panaxginseng C. A. Mey.的干燥根及根茎。主要化学成分包括皂苷、多糖、聚炔醇、挥发油、蛋白质、多肽、氨基酸等。在总结人参调节免疫功能的化学成分和药理作用的基础上,基于质量标志物(Quality marker,Q-Marker)原则从植物亲缘性,化学成分有效性,特有性和复方配伍等方面进行预测分析。大类成分以人参皂苷、多糖、蛋白质、挥发油为人参调节免疫功能的质量标志物,单一成分可选取人参皂苷Rg1、Re、Rb1、Rg3、Rh1、Rh2、Rd、CK、Ro、Rg5、人参D-葡萄糖、半乳糖、阿拉伯糖、人参炔醇作为备选物质,为其提供一定的质量控制方法参考。

, authors=徐慧1, 冉靖1, 王丹2, 张巍1, 白雪媛1, authorsList=徐慧, 冉靖, 王丹, 张巍, 白雪媛, authorCompany=null, correspAuthors=张巍, 白雪媛, authorNote=

徐慧(2001-),女,贵州铜仁人,硕士,研究方向:中药有效成分发现、生物转化及健康产品研究与开发。

, correspAuthorsNote=
张巍(1980-),男,吉林长春人,副研究员,硕士研究生导师,博士,研究方向:中药分析新方法与新技术。E-mail:。
白雪媛(1980-),女,吉林长春人,研究员,博士研究生导师,硕士,研究方向:中药传统功效生物学机制研究及产品开发。E-mail:。
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徐慧(2001-),女,贵州铜仁人,硕士,研究方向:中药有效成分发现、生物转化及健康产品研究与开发。

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徐慧(2001-),女,贵州铜仁人,硕士,研究方向:中药有效成分发现、生物转化及健康产品研究与开发。

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编号化学成分分子式参考文献
1Rg1C42H72O14[6]
2Rg3C42H72O13[7-8]
3Rb1C54H92O23[9-10]
4Rh1C36H62O9[11]
5Rh2C36H62O8[12-13]
6ReC48H82O18[14-15]
7RdC48H82O18[4]
8CKC36H62O8[16]
9RoC48H76O19[17]
10Rg5C42H70O12[18]
), ArticleFig(id=1322923627968082853, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=CN, label=表1, caption=

人参调节免疫功能的主要皂苷类成分

, figureFileSmall=null, figureFileBig=null, tableContent=
编号化学成分分子式参考文献
1Rg1C42H72O14[6]
2Rg3C42H72O13[7-8]
3Rb1C54H92O23[9-10]
4Rh1C36H62O9[11]
5Rh2C36H62O8[12-13]
6ReC48H82O18[14-15]
7RdC48H82O18[4]
8CKC36H62O8[16]
9RoC48H76O19[17]
10Rg5C42H70O12[18]
), ArticleFig(id=1322923628060357542, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=EN, label=null, caption=null, figureFileSmall=null, figureFileBig=null, tableContent=
编号化学成分分子式参考文献
11葡萄糖C6H12O6[20]
12阿拉伯糖C5H10O5[20]
13半乳糖C20H31N3O12[20]
14鼠李糖C6H14O6[20]
15半乳糖醛酸C18H26O19[20]
16葡萄糖醛酸C6H10O7[20]
17甘露糖C6H14O6[22]
), ArticleFig(id=1322923628140049319, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=CN, label=表2, caption=

人参调节免疫功能的主要多糖类成分

, figureFileSmall=null, figureFileBig=null, tableContent=
编号化学成分分子式参考文献
11葡萄糖C6H12O6[20]
12阿拉伯糖C5H10O5[20]
13半乳糖C20H31N3O12[20]
14鼠李糖C6H14O6[20]
15半乳糖醛酸C18H26O19[20]
16葡萄糖醛酸C6H10O7[20]
17甘露糖C6H14O6[22]
), ArticleFig(id=1322923628198769576, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=EN, label=null, caption=null, figureFileSmall=null, figureFileBig=null, tableContent=
化学成分相关疾病作用机制参考文献
Rg3肿瘤化疗增加人类白细胞抗原DR(Human leukocyte antigen DR,HLA-DR)、人类白细胞抗原ABC(Human leukocyte antigen ABC,HLA-ABC)、CD3-CD56+16等分子表达,使CD4+/CD8+及辅助性T细胞1(T helper cell 1,Th1)/辅助性T细胞2(T helper cell 2,Th2)向免疫增强的方向漂移[27]
鼻咽癌促进Th1/Th2细胞平衡,抑制血管内皮生长因子(Vascular endothelial growth factor,VEGF)产生与表达[28]
溃疡性结肠炎通过调节Th1与Th2细胞因子表达,促进Th1/Th2平衡,抑制核转录因子-kappa B(nuclear factor-kappa B,NF-κB)活化[29-30]
黑色素瘤激活丝裂原激活蛋白激酶(Mitogen-activated protein kinase,MAPK)/细胞外信号调节激酶(Extracellular Signal-Regulated Kinases,ERK)通路促进CD8 T淋巴细胞的杀伤性作用[31]
神经炎症通过负调控CD4 T细胞中维甲酸相关孤儿受体γ t(RetinoicAcid-related Orphangammat,ROR-γ t)的表达,进而阻碍辅助性T细胞17(T helpercell 1,Th17)细胞分化和Th17介导的神经炎症[32]
甲状腺炎调控CD3CD8白介素-4(Interleukin-4,IL-4)和CD3CD8伽马干扰素(Interferon-γ,IFN-γ)辅助T淋巴细胞频率而降低IL-4和IFN-γ的分泌[33]
胃癌使患者体内CD3+、CD4+、T淋巴细胞转化率及CD4+/CD8+值均上升,且CD8+值下降[34]
关节炎调节氧化磷酸化途径和增强CD4(+)CD25(+)叉头翼状螺旋转录因子3(Forkhead box protein 3,FOXP3)(+)调节性T细胞(Regulatory Tcell,Treg)细胞维持类风湿性关节炎(RheumatoidArthritis,RA)小鼠外周免疫耐受的功能[35]
肺癌降低化疗耐药诱导的程序性死亡蛋白配体-1(Programmed death ligand-1,PD-L1)表达,恢复T细胞对癌细胞的细胞毒素[36]
Rg1溃疡性结肠炎发挥程序性细胞死亡蛋白-1(Programmed cell death-1,PD-1)/PD-L1抑制作用,通过调控Treg/辅助性T细胞9(T helper cell 9,Th9)平衡而有效改善实验性小鼠的结肠炎[37]
结肠炎通过抑制脂多糖(Lipopolysaccharides,LPS)与巨噬细胞上Toll样受体4(Toll-like receptor 4,TLR4)的结合并恢复Th17/Treg失衡来改善结肠炎[38]
脑脊髓炎通过抑制Th17、Th1细胞及其分泌的炎症细胞因子而调控Treg细胞失衡,抑制中枢神经系统炎症过度激活[39]
系统性红斑狼疮调节T细胞活化和Th1/Th2平衡[40]
抗念珠菌病通过由Th4显性细胞因子反应导致的CD1+T细胞介导的免疫反应帮助宿主抵抗播散性念珠菌病[41]
脓毒血症显著提高体外淋巴细胞的活性,显著促进刀豆蛋白A(Con A)诱导下淋巴细胞的增殖,T细胞表面活化分子CD69、CD25、CD71的表达及淋巴细胞线粒体膜电势的升高,以及促进淋巴细胞增殖于S期[42]
抗疲劳调节体内T细胞亚群的数量,增强免疫力,对抗疲劳[43]
肝炎通过抑制促炎反应降低肝损伤的发生率,抑制CD4+和CD8+T淋巴细胞向肝脏的募集[44]
Ⅲ型前列腺炎降低Ⅲ型前列腺炎模型中异常增高的IL-4、肿瘤坏死因子-α(Tumor necrosis factor-alpha,TNF-α)水平,减轻前列腺的损伤,通过信号传导通路促进T细胞增殖,进而产生较多细胞因子[45]
抗病毒通过由Th4显性细胞因子反应导致的CD1+T细胞介导免疫反应[41]
败血症增强CD4tT淋巴细胞的活性,保护胸腺和脾脏中的免疫细胞免于凋亡[46]
Rh1抗哮喘调节Th1/Th2细胞因子平衡,减轻小鼠模型中卵白蛋白(Oval albumin,OVA)诱导的哮喘[47]
Re抗念珠菌病通过刺激CD4+T细胞来操纵Th1/Th2分化[48]
Rh2抗结肠腺癌促进T细胞浸润和活化增强了PD-L1阻断的抗癌作用[49]
银屑病通过抑制血管通透性来显著减少T细胞的浸润[50]
抗荷瘤增加肿瘤坏死因子受体相关因子6(Tumour necrosis factor receptor associated factor 6,TRAF6)的表达,抑制Tlr65小鼠核内NF-κBp4水平[51]
白血病抑制磷脂酰肌醇3激酶(Phosphoinositide 3-kinase,PI3K)/蛋白激酶B(Protein kinase B,Akt)/雷帕霉素靶蛋白(Mammalian target of rapamycin,mTOR)信号通路,发挥抗急性淋巴细胞白血病作用[52]
抗哮喘通过抑制磷酸化AKT、p38MAPK和NF-κB信号通路而实现抗哮喘作用[53]
Rb1抗哮喘降级Th1/Th2[54]
抗细胞凋亡显著逆转了脱氧雪腐镰刀菌烯醇诱导的T细胞亚群百分比、细胞因子水平和免疫球蛋白的产生[55]
重症肌无力降低单核细胞(MNCs)中Th17细胞的百分比,增加MNCs中Treg和Th2细胞的数量[56]
系统性红斑狼疮抑制ConA刺激的系统性红斑狼疮患者外周血T淋巴细胞增殖活性,增加CD4CD25T细胞比例,维持Th1/Th2免疫平衡[57]
再生障碍性贫血增加CD4/CD8比例、降低Th1型细胞因子IFN-γ分泌、促进CD34+干细胞生长[58]
Rd脑脊髓炎调节IFN-γ和IL-4的分泌,促进体内(大脑皮层)和体外(脾细胞培养上清液)Th2转移[59]
人参多糖创伤性脓毒症使HLA-DR、CD4+细胞分数、CD4+/CD8+比值、NK百分率升高,CD8+细胞分数降低[60]
慢性肾功能衰竭促进体外T细胞的转化和IL-2(Interleukin-2,IL-2)诱生能力[61]
乳腺癌CD3+、CD4+、CD++1656的比例均出现了下降,而CD8+的比例出现了上升[62]
抗肺癌有效调节Th1/Th2免疫平衡。可能是因为人参多糖注射液可调控多种抗肿瘤细胞因子的释放,发挥免疫调节作用[63]
脑脊髓炎通过抑制自身反应性T细胞的增殖和炎性细胞因子的产生来显著改善该免疫疾病。此外,人参通过激活转录因子Foxp3促进免疫抑制Tregs的产生。[64]
非小细胞肺癌Th1细胞因子(INF-γ、IL-2)表达增加和Th1/Th2比值[INF-γ/IL-4、IL-2/白细胞介素(IL-5)]以及FACT-L评分和Th2细胞因子(IL-4、IL-5)表达降低[65]
放射防护人参处理的骨髓细胞的主要组织相容性复合物Ⅱ(Major histocompatibility complexⅡ,MHC-Ⅱ)类分子的表达增加,同时显示出更高的同种异体CD4+T淋巴细胞增殖水平[66]
黑色素瘤通过内源产生的多种细胞因子从NK和T细胞中产生LAK细胞[67]
), ArticleFig(id=1322923628278461354, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=CN, label=表3, caption=

人参调节T淋巴细胞治疗免疫相关疾病及作用机制

, figureFileSmall=null, figureFileBig=null, tableContent=
化学成分相关疾病作用机制参考文献
Rg3肿瘤化疗增加人类白细胞抗原DR(Human leukocyte antigen DR,HLA-DR)、人类白细胞抗原ABC(Human leukocyte antigen ABC,HLA-ABC)、CD3-CD56+16等分子表达,使CD4+/CD8+及辅助性T细胞1(T helper cell 1,Th1)/辅助性T细胞2(T helper cell 2,Th2)向免疫增强的方向漂移[27]
鼻咽癌促进Th1/Th2细胞平衡,抑制血管内皮生长因子(Vascular endothelial growth factor,VEGF)产生与表达[28]
溃疡性结肠炎通过调节Th1与Th2细胞因子表达,促进Th1/Th2平衡,抑制核转录因子-kappa B(nuclear factor-kappa B,NF-κB)活化[29-30]
黑色素瘤激活丝裂原激活蛋白激酶(Mitogen-activated protein kinase,MAPK)/细胞外信号调节激酶(Extracellular Signal-Regulated Kinases,ERK)通路促进CD8 T淋巴细胞的杀伤性作用[31]
神经炎症通过负调控CD4 T细胞中维甲酸相关孤儿受体γ t(RetinoicAcid-related Orphangammat,ROR-γ t)的表达,进而阻碍辅助性T细胞17(T helpercell 1,Th17)细胞分化和Th17介导的神经炎症[32]
甲状腺炎调控CD3CD8白介素-4(Interleukin-4,IL-4)和CD3CD8伽马干扰素(Interferon-γ,IFN-γ)辅助T淋巴细胞频率而降低IL-4和IFN-γ的分泌[33]
胃癌使患者体内CD3+、CD4+、T淋巴细胞转化率及CD4+/CD8+值均上升,且CD8+值下降[34]
关节炎调节氧化磷酸化途径和增强CD4(+)CD25(+)叉头翼状螺旋转录因子3(Forkhead box protein 3,FOXP3)(+)调节性T细胞(Regulatory Tcell,Treg)细胞维持类风湿性关节炎(RheumatoidArthritis,RA)小鼠外周免疫耐受的功能[35]
肺癌降低化疗耐药诱导的程序性死亡蛋白配体-1(Programmed death ligand-1,PD-L1)表达,恢复T细胞对癌细胞的细胞毒素[36]
Rg1溃疡性结肠炎发挥程序性细胞死亡蛋白-1(Programmed cell death-1,PD-1)/PD-L1抑制作用,通过调控Treg/辅助性T细胞9(T helper cell 9,Th9)平衡而有效改善实验性小鼠的结肠炎[37]
结肠炎通过抑制脂多糖(Lipopolysaccharides,LPS)与巨噬细胞上Toll样受体4(Toll-like receptor 4,TLR4)的结合并恢复Th17/Treg失衡来改善结肠炎[38]
脑脊髓炎通过抑制Th17、Th1细胞及其分泌的炎症细胞因子而调控Treg细胞失衡,抑制中枢神经系统炎症过度激活[39]
系统性红斑狼疮调节T细胞活化和Th1/Th2平衡[40]
抗念珠菌病通过由Th4显性细胞因子反应导致的CD1+T细胞介导的免疫反应帮助宿主抵抗播散性念珠菌病[41]
脓毒血症显著提高体外淋巴细胞的活性,显著促进刀豆蛋白A(Con A)诱导下淋巴细胞的增殖,T细胞表面活化分子CD69、CD25、CD71的表达及淋巴细胞线粒体膜电势的升高,以及促进淋巴细胞增殖于S期[42]
抗疲劳调节体内T细胞亚群的数量,增强免疫力,对抗疲劳[43]
肝炎通过抑制促炎反应降低肝损伤的发生率,抑制CD4+和CD8+T淋巴细胞向肝脏的募集[44]
Ⅲ型前列腺炎降低Ⅲ型前列腺炎模型中异常增高的IL-4、肿瘤坏死因子-α(Tumor necrosis factor-alpha,TNF-α)水平,减轻前列腺的损伤,通过信号传导通路促进T细胞增殖,进而产生较多细胞因子[45]
抗病毒通过由Th4显性细胞因子反应导致的CD1+T细胞介导免疫反应[41]
败血症增强CD4tT淋巴细胞的活性,保护胸腺和脾脏中的免疫细胞免于凋亡[46]
Rh1抗哮喘调节Th1/Th2细胞因子平衡,减轻小鼠模型中卵白蛋白(Oval albumin,OVA)诱导的哮喘[47]
Re抗念珠菌病通过刺激CD4+T细胞来操纵Th1/Th2分化[48]
Rh2抗结肠腺癌促进T细胞浸润和活化增强了PD-L1阻断的抗癌作用[49]
银屑病通过抑制血管通透性来显著减少T细胞的浸润[50]
抗荷瘤增加肿瘤坏死因子受体相关因子6(Tumour necrosis factor receptor associated factor 6,TRAF6)的表达,抑制Tlr65小鼠核内NF-κBp4水平[51]
白血病抑制磷脂酰肌醇3激酶(Phosphoinositide 3-kinase,PI3K)/蛋白激酶B(Protein kinase B,Akt)/雷帕霉素靶蛋白(Mammalian target of rapamycin,mTOR)信号通路,发挥抗急性淋巴细胞白血病作用[52]
抗哮喘通过抑制磷酸化AKT、p38MAPK和NF-κB信号通路而实现抗哮喘作用[53]
Rb1抗哮喘降级Th1/Th2[54]
抗细胞凋亡显著逆转了脱氧雪腐镰刀菌烯醇诱导的T细胞亚群百分比、细胞因子水平和免疫球蛋白的产生[55]
重症肌无力降低单核细胞(MNCs)中Th17细胞的百分比,增加MNCs中Treg和Th2细胞的数量[56]
系统性红斑狼疮抑制ConA刺激的系统性红斑狼疮患者外周血T淋巴细胞增殖活性,增加CD4CD25T细胞比例,维持Th1/Th2免疫平衡[57]
再生障碍性贫血增加CD4/CD8比例、降低Th1型细胞因子IFN-γ分泌、促进CD34+干细胞生长[58]
Rd脑脊髓炎调节IFN-γ和IL-4的分泌,促进体内(大脑皮层)和体外(脾细胞培养上清液)Th2转移[59]
人参多糖创伤性脓毒症使HLA-DR、CD4+细胞分数、CD4+/CD8+比值、NK百分率升高,CD8+细胞分数降低[60]
慢性肾功能衰竭促进体外T细胞的转化和IL-2(Interleukin-2,IL-2)诱生能力[61]
乳腺癌CD3+、CD4+、CD++1656的比例均出现了下降,而CD8+的比例出现了上升[62]
抗肺癌有效调节Th1/Th2免疫平衡。可能是因为人参多糖注射液可调控多种抗肿瘤细胞因子的释放,发挥免疫调节作用[63]
脑脊髓炎通过抑制自身反应性T细胞的增殖和炎性细胞因子的产生来显著改善该免疫疾病。此外,人参通过激活转录因子Foxp3促进免疫抑制Tregs的产生。[64]
非小细胞肺癌Th1细胞因子(INF-γ、IL-2)表达增加和Th1/Th2比值[INF-γ/IL-4、IL-2/白细胞介素(IL-5)]以及FACT-L评分和Th2细胞因子(IL-4、IL-5)表达降低[65]
放射防护人参处理的骨髓细胞的主要组织相容性复合物Ⅱ(Major histocompatibility complexⅡ,MHC-Ⅱ)类分子的表达增加,同时显示出更高的同种异体CD4+T淋巴细胞增殖水平[66]
黑色素瘤通过内源产生的多种细胞因子从NK和T细胞中产生LAK细胞[67]
), ArticleFig(id=1322923628370736043, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=EN, label=null, caption=null, figureFileSmall=null, figureFileBig=null, tableContent=
化学成分相关疾病作用机制参考文献
Rg3骨髓癌上调B细胞淋巴瘤-2相关X蛋白(Bax)的表达,诱导多发性骨髓瘤细胞凋亡[68]
系统性红斑狼疮抑制B细胞增殖,减少B细胞分泌物免疫球蛋白G(Immunoglobulin G,IgG)和免疫球蛋白M(Immunoglobulin M,IgM)的分泌,提升B细胞凋亡相关蛋白和抑制B细胞相关因子的表达[69]
Rh1系统性红斑狼疮抑制B细胞增殖,减少B细胞分泌物IgG和IgM的分泌,提升B细胞凋亡相关蛋白和抑制B细胞相关因子的表达[69]
Rg1系统性红斑狼疮抑制B细胞增殖,减少B细胞分泌物IgG和IgM的分泌,提升B细胞凋亡相关蛋白和抑制B细胞相关因子的表达[69]
Rb1系统性红斑狼疮抑制B细胞增殖,减少B细胞分泌物IgG和IgM的分泌,提升B细胞凋亡相关蛋白和抑制B细胞相关因子的表达[69]
CK关节炎以β抑制因子1(β-arrestin1)-AP2依赖性方式触发免疫球蛋白D(MmunoglobulinD,Ig D)-B细胞受体(B cell receptor,BCR)内化来抑制B细胞活化[70]
), ArticleFig(id=1322923628458816428, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=CN, label=表4, caption=

人参调节B淋巴细胞治疗免疫相关疾病及作用机制

, figureFileSmall=null, figureFileBig=null, tableContent=
化学成分相关疾病作用机制参考文献
Rg3骨髓癌上调B细胞淋巴瘤-2相关X蛋白(Bax)的表达,诱导多发性骨髓瘤细胞凋亡[68]
系统性红斑狼疮抑制B细胞增殖,减少B细胞分泌物免疫球蛋白G(Immunoglobulin G,IgG)和免疫球蛋白M(Immunoglobulin M,IgM)的分泌,提升B细胞凋亡相关蛋白和抑制B细胞相关因子的表达[69]
Rh1系统性红斑狼疮抑制B细胞增殖,减少B细胞分泌物IgG和IgM的分泌,提升B细胞凋亡相关蛋白和抑制B细胞相关因子的表达[69]
Rg1系统性红斑狼疮抑制B细胞增殖,减少B细胞分泌物IgG和IgM的分泌,提升B细胞凋亡相关蛋白和抑制B细胞相关因子的表达[69]
Rb1系统性红斑狼疮抑制B细胞增殖,减少B细胞分泌物IgG和IgM的分泌,提升B细胞凋亡相关蛋白和抑制B细胞相关因子的表达[69]
CK关节炎以β抑制因子1(β-arrestin1)-AP2依赖性方式触发免疫球蛋白D(MmunoglobulinD,Ig D)-B细胞受体(B cell receptor,BCR)内化来抑制B细胞活化[70]
), ArticleFig(id=1322923628530119597, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=EN, label=null, caption=null, figureFileSmall=null, figureFileBig=null, tableContent=
化学成分相关疾病作用机制参考文献
Rg1肺纤维化降低肝纤维化小鼠肝脏中的吲哚胺-2,3-双加氧酶1(Indoleamine-2,3-dioxygenase1,IDO1)蛋白表达水平,提高肝纤维化小鼠肝脏中DDCs免疫表型的成熟[74]
Rg3肾癌Rg3促进DC分化,MHC-Ⅱ的增强使DC获得更强的抗原摄取能力,刺激细胞毒性T淋巴细胞的免疫反应[75]
Rb1再生障碍性贫血抑制树突状细胞的成熟,调节CD4+T细胞/CD8+T细胞比例[76]
Ro白血病转录活化子5(Signaltrans-ducer and activators of transcription 5,STAT5)信号通路可能是人参皂苷Ro促进白血病源DC的关键机制之一[77]
Rh2胰腺癌吉西他滨(GEM)-Rh2可能通过增强肿瘤免疫原性和降低免疫抑制因子水平,通过胱天蛋白酶募集域蛋白9(Caspase recruitment domain-containing protein 9,CARD9)-B细胞淋巴瘤因子10(B cell lymphoma/leukemia 10,BCL10)-泪腺黏膜相关淋巴组织淋巴瘤1(Mucosa-associated Lymphoid Tissue Lymphoma,MALT1)/NF-κB通路重新激活DC细胞[78]
), ArticleFig(id=1322923628614005679, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=CN, label=表5, caption=

人参调节树突状细胞治疗免疫相关疾病及作用机制

, figureFileSmall=null, figureFileBig=null, tableContent=
化学成分相关疾病作用机制参考文献
Rg1肺纤维化降低肝纤维化小鼠肝脏中的吲哚胺-2,3-双加氧酶1(Indoleamine-2,3-dioxygenase1,IDO1)蛋白表达水平,提高肝纤维化小鼠肝脏中DDCs免疫表型的成熟[74]
Rg3肾癌Rg3促进DC分化,MHC-Ⅱ的增强使DC获得更强的抗原摄取能力,刺激细胞毒性T淋巴细胞的免疫反应[75]
Rb1再生障碍性贫血抑制树突状细胞的成熟,调节CD4+T细胞/CD8+T细胞比例[76]
Ro白血病转录活化子5(Signaltrans-ducer and activators of transcription 5,STAT5)信号通路可能是人参皂苷Ro促进白血病源DC的关键机制之一[77]
Rh2胰腺癌吉西他滨(GEM)-Rh2可能通过增强肿瘤免疫原性和降低免疫抑制因子水平,通过胱天蛋白酶募集域蛋白9(Caspase recruitment domain-containing protein 9,CARD9)-B细胞淋巴瘤因子10(B cell lymphoma/leukemia 10,BCL10)-泪腺黏膜相关淋巴组织淋巴瘤1(Mucosa-associated Lymphoid Tissue Lymphoma,MALT1)/NF-κB通路重新激活DC细胞[78]
), ArticleFig(id=1322923628672725936, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=EN, label=null, caption=null, figureFileSmall=null, figureFileBig=null, tableContent=
化学成分相关疾病作用机制参考文献
Rb1卵巢癌人参皂苷Rb1不能直接活化NK细胞,但是能拮抗达沙替尼通过NK细胞对卵巢癌细胞抑制效应[82]
抗肝癌人参皂苷Rb1通过拮抗人肝癌细胞(Human hepatocellular carcinomas,HepG2)对NK细胞的免疫抑制[83]
Rg3宫颈癌20(R)-Rg3通过激活MAPK/ERK通路促进NK细胞活性[84]
前列腺癌20(R)-Rg3通过激活MAPK/ERK通路促进NK细胞活性[84]
肺癌20(R)-Rg3通过激活MAPK/ERK通路促进NK细胞活性[84]
胰腺癌20(R)-Rg3通过激活MAPK/ERK通路促进NK细胞活性[84]
Rh2乳腺癌Rh2通过抑制内质网蛋白5(Endoplasmic reticulum protein 5,ERp5)表达,减少主要MHCI.类链相关分子(MHC classI chain-related molecule A,MICA)的脱落,从而干预乳腺癌的免疫逃逸,增强NK细胞的细胞毒作用,促进NK细胞对乳腺癌的免疫监视功能[12]
人参多糖抑制肿瘤转移白介素-12(Interleukin-12,IL-12)在动物模型中显示出强大的抗肿瘤和抗转移活性,并通过激活效应细胞来诱导。IL-12的作用很可能是由IFN-γ介导的,主要在NK细胞中[85]
), ArticleFig(id=1322923630384001970, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=CN, label=表6, caption=

人参调节NK细胞的免疫相关疾病及作用机制

, figureFileSmall=null, figureFileBig=null, tableContent=
化学成分相关疾病作用机制参考文献
Rb1卵巢癌人参皂苷Rb1不能直接活化NK细胞,但是能拮抗达沙替尼通过NK细胞对卵巢癌细胞抑制效应[82]
抗肝癌人参皂苷Rb1通过拮抗人肝癌细胞(Human hepatocellular carcinomas,HepG2)对NK细胞的免疫抑制[83]
Rg3宫颈癌20(R)-Rg3通过激活MAPK/ERK通路促进NK细胞活性[84]
前列腺癌20(R)-Rg3通过激活MAPK/ERK通路促进NK细胞活性[84]
肺癌20(R)-Rg3通过激活MAPK/ERK通路促进NK细胞活性[84]
胰腺癌20(R)-Rg3通过激活MAPK/ERK通路促进NK细胞活性[84]
Rh2乳腺癌Rh2通过抑制内质网蛋白5(Endoplasmic reticulum protein 5,ERp5)表达,减少主要MHCI.类链相关分子(MHC classI chain-related molecule A,MICA)的脱落,从而干预乳腺癌的免疫逃逸,增强NK细胞的细胞毒作用,促进NK细胞对乳腺癌的免疫监视功能[12]
人参多糖抑制肿瘤转移白介素-12(Interleukin-12,IL-12)在动物模型中显示出强大的抗肿瘤和抗转移活性,并通过激活效应细胞来诱导。IL-12的作用很可能是由IFN-γ介导的,主要在NK细胞中[85]
), ArticleFig(id=1322923630597911476, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=EN, label=null, caption=null, figureFileSmall=null, figureFileBig=null, tableContent=
化学成分相关疾病作用机制参考文献
Rh2肺癌IFN与G-Rh2作为第一启动信号在第二信号(如脂多糖)的协同下,诱导MHC-Ⅱ类抗原及Fc受体表达,调节TNF-α,NO和IL-1等活性物质的生成[89]
抗炎抑制LPS刺激的巨噬细胞中的炎症反应[90]
肝纤维化Rh2通过调节炎症相关基因来抑制巨噬细胞募集从而抑制肝纤维化。[91]
Rb1抗炎阻断LPS与肺泡巨噬细胞膜的结合,抑制LPS诱导的细胞内核转录因子抑制蛋白(IκB)低表达,从而使TNFα分泌水平下降[92]
动脉粥样硬化Rb1通过促进IL-4/白介素-13(Interleukin-13,IL-13)分泌诱导M2巨噬细胞极化,也可通过诱导M2巨噬细胞极化增加动脉粥样硬化斑块的稳定性[93]
脊髓损伤通过调节巨噬细胞/小胶质细胞的极化、减轻炎症反应而促进大鼠脊髓损伤后神经功能的恢复。[94]
心脏肥大降低丝裂原活化蛋白激酶(MAPKs)和丝裂原活化蛋白激酶1/2(Mitogen kinase 1and 2,MEK1/2)的磷酸化,并减少炎症介质的产生,抑制LPS或血管紧张素Ⅱ(Angiotensin-Ⅱ,Ang-Ⅱ)刺激的巨噬细胞中促肥厚microRNA-155(miR-155)的表达[90]
CK抗炎诱导单核细胞趋化因子-1(Monocyte chemokine-1,MCP-1)和TNF-α升高,促进白介素-10(Interleukin-10,IL-10)表达,抑制炎性巨噬细胞活化,增加抗炎巨噬细胞表达[95]
抗肥胖通过激活过氧化物酶体增殖物激活受体γ(Peroxisome proliferatoractivated receptorγ,PPARγ),调节巨噬细胞募集和极化[96]
骨质疏松症通过抑制NF-κB信号通路,降低破骨细胞生成并防止去卵巢骨质疏松模型大鼠诱导的骨流失[97-98]
关节炎抑制巨噬细胞吞噬,降低M1比例。降低胶原诱导性关节炎(Collagen-induced arthritis,CIA)小鼠巨噬细胞中过表达的β-arrestin2、抑制型G蛋白α(Gαi)、TLR4和NF-κB,同时增加激动型G蛋白α(Gαs)的表达。此外,CK通过巨噬细胞中的β-arrestin2调节,促进TLR4-Gαs偶联并抑制TLR4-Gαi偶联[99]
耳皮炎调节巨噬细胞产生的环氧合酶-2(Cyclooxygenase,COX-2)和Th细胞诱导的干扰素-γ和IL-4。[100]
Rb1肺纤维化巨噬细胞中NOD样受体热蛋白结构域相关蛋白3(NOD-like receptor thermal protein domain associated protein 3,NLRP3)炎症小体激活后分泌的白细胞介素-1β(Interleukin-1β,IL-1β),促进成纤维细胞分化。Rb1抑制脂多糖和三磷酸腺苷诱导的巨噬细胞中NLRP3炎症小体活化,并干扰巨噬细胞和成纤维细胞之间的串扰[101]
抗病毒抑制脂多糖/环己酰亚胺诱导的D3转导巨噬细胞中的AKT和糖原合酶激酶-3β磷酸化,但不抑制磷酸肌醇依赖性蛋白激酶1(Phosphoinositide dependent protein kinase 1,PDK-1)和磷酸肌醇-3-激酶(Phosphoinositide 3-kinase,PI3K)的磷酸化[102]
Rd肾缺血再灌注损伤通过下调M1巨噬细胞极化,对肾缺血/再灌注损伤具有保护功能[103]
心肌梗死人参皂苷Rd促进Ly6C的转化高MOS/MPS为Ly6C低心肌梗死后小鼠的Mos/Mps,通过激活AKT/mTOR信号通路,抑制心功能障碍,促进心脏修复[104]
Rg1结肠炎人参皂苷Rg1通过调节M1/M2巨噬细胞极化和微生物群组成来改善结肠炎,通过抑制Nogo-B/RhoA信号通路完成[105]
创伤性脑损伤Rg1降低IL-1β诱导的巨噬细胞(IIM)-Exos-miR-21(RIIM-Exos)中miR-21-5p的含量。Rg1可以抑制外周血流向脑Exos-miR-21的释放,增强基质金属蛋白酶组织抑制剂(Tissue inhibitors of matrix metalloproteinases,TIMPs)表达、基质金属蛋白酶(Matrix metalloproteinases,MMPs)水解,限制致结蛋白降解,从而保护神经炎症和血脑屏障的完整性[106]
糖尿病性心肌病RG1诱导的间充质干细胞分泌的外泌体circNOTCH1可以通过激活NOTCH信号通路,诱导巨噬细胞M2极化来缓解糖尿病性心肌病(Diabetic cardiomyopathy,DCM)[107]
脓毒症抑制mRNA表达和促炎介质的产生,包括肿瘤坏死因子α、白细胞介素-1β、白细胞介素-6、cox-2和LPS刺激的巨噬细胞诱导的一氧化氮合酶[108]
Rg5肺部炎症抑制LPS与巨噬细胞上的toll样受体-4的结合[109]
特应性皮炎下调人角质形成细胞和巨噬细胞中NF-κB/p38MAPK/STAT1信号传导,减弱TNF-α/IFN-γ诱导的胸腺活化调节趋化因子(Thymus andactivation regulated chemokine,TARC)/CCL17的产生和LPS诱导的NO产生[110]
Rg3视网膜缺血再灌注缓解氧化应激和促进小胶质细胞/巨噬细胞M2极化[111]
人参多糖关节炎使Peyer's结淋巴细胞(Lymphocytes of Peyer's patch,PPL)分泌TNF-α,使IFN-γ的分泌增加,而上皮内淋巴细胞(Intraepithelial lymphocytes,IELs)和固有层淋巴细胞(Lamina propria lymphocytes,LPLs)所分泌的TNF-α和IFN-γ的水平均有不同程度地降低[112]
人参挥发油抗炎抑制巨噬细胞的TNF-α、IL-6和IL-1β蛋白质分泌量及IImRNA的表达水平[26]
胃癌通过作用表皮生长因子受体(Epidermal growth factor receptor,EGFR)、MAPK1、MAPK3和IL-6这几个靶点来实现治疗胃癌作用[113]
), ArticleFig(id=1322923630698574773, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=CN, label=表7, caption=

人参调节巨噬细胞的免疫相关疾病及作用机制

, figureFileSmall=null, figureFileBig=null, tableContent=
化学成分相关疾病作用机制参考文献
Rh2肺癌IFN与G-Rh2作为第一启动信号在第二信号(如脂多糖)的协同下,诱导MHC-Ⅱ类抗原及Fc受体表达,调节TNF-α,NO和IL-1等活性物质的生成[89]
抗炎抑制LPS刺激的巨噬细胞中的炎症反应[90]
肝纤维化Rh2通过调节炎症相关基因来抑制巨噬细胞募集从而抑制肝纤维化。[91]
Rb1抗炎阻断LPS与肺泡巨噬细胞膜的结合,抑制LPS诱导的细胞内核转录因子抑制蛋白(IκB)低表达,从而使TNFα分泌水平下降[92]
动脉粥样硬化Rb1通过促进IL-4/白介素-13(Interleukin-13,IL-13)分泌诱导M2巨噬细胞极化,也可通过诱导M2巨噬细胞极化增加动脉粥样硬化斑块的稳定性[93]
脊髓损伤通过调节巨噬细胞/小胶质细胞的极化、减轻炎症反应而促进大鼠脊髓损伤后神经功能的恢复。[94]
心脏肥大降低丝裂原活化蛋白激酶(MAPKs)和丝裂原活化蛋白激酶1/2(Mitogen kinase 1and 2,MEK1/2)的磷酸化,并减少炎症介质的产生,抑制LPS或血管紧张素Ⅱ(Angiotensin-Ⅱ,Ang-Ⅱ)刺激的巨噬细胞中促肥厚microRNA-155(miR-155)的表达[90]
CK抗炎诱导单核细胞趋化因子-1(Monocyte chemokine-1,MCP-1)和TNF-α升高,促进白介素-10(Interleukin-10,IL-10)表达,抑制炎性巨噬细胞活化,增加抗炎巨噬细胞表达[95]
抗肥胖通过激活过氧化物酶体增殖物激活受体γ(Peroxisome proliferatoractivated receptorγ,PPARγ),调节巨噬细胞募集和极化[96]
骨质疏松症通过抑制NF-κB信号通路,降低破骨细胞生成并防止去卵巢骨质疏松模型大鼠诱导的骨流失[97-98]
关节炎抑制巨噬细胞吞噬,降低M1比例。降低胶原诱导性关节炎(Collagen-induced arthritis,CIA)小鼠巨噬细胞中过表达的β-arrestin2、抑制型G蛋白α(Gαi)、TLR4和NF-κB,同时增加激动型G蛋白α(Gαs)的表达。此外,CK通过巨噬细胞中的β-arrestin2调节,促进TLR4-Gαs偶联并抑制TLR4-Gαi偶联[99]
耳皮炎调节巨噬细胞产生的环氧合酶-2(Cyclooxygenase,COX-2)和Th细胞诱导的干扰素-γ和IL-4。[100]
Rb1肺纤维化巨噬细胞中NOD样受体热蛋白结构域相关蛋白3(NOD-like receptor thermal protein domain associated protein 3,NLRP3)炎症小体激活后分泌的白细胞介素-1β(Interleukin-1β,IL-1β),促进成纤维细胞分化。Rb1抑制脂多糖和三磷酸腺苷诱导的巨噬细胞中NLRP3炎症小体活化,并干扰巨噬细胞和成纤维细胞之间的串扰[101]
抗病毒抑制脂多糖/环己酰亚胺诱导的D3转导巨噬细胞中的AKT和糖原合酶激酶-3β磷酸化,但不抑制磷酸肌醇依赖性蛋白激酶1(Phosphoinositide dependent protein kinase 1,PDK-1)和磷酸肌醇-3-激酶(Phosphoinositide 3-kinase,PI3K)的磷酸化[102]
Rd肾缺血再灌注损伤通过下调M1巨噬细胞极化,对肾缺血/再灌注损伤具有保护功能[103]
心肌梗死人参皂苷Rd促进Ly6C的转化高MOS/MPS为Ly6C低心肌梗死后小鼠的Mos/Mps,通过激活AKT/mTOR信号通路,抑制心功能障碍,促进心脏修复[104]
Rg1结肠炎人参皂苷Rg1通过调节M1/M2巨噬细胞极化和微生物群组成来改善结肠炎,通过抑制Nogo-B/RhoA信号通路完成[105]
创伤性脑损伤Rg1降低IL-1β诱导的巨噬细胞(IIM)-Exos-miR-21(RIIM-Exos)中miR-21-5p的含量。Rg1可以抑制外周血流向脑Exos-miR-21的释放,增强基质金属蛋白酶组织抑制剂(Tissue inhibitors of matrix metalloproteinases,TIMPs)表达、基质金属蛋白酶(Matrix metalloproteinases,MMPs)水解,限制致结蛋白降解,从而保护神经炎症和血脑屏障的完整性[106]
糖尿病性心肌病RG1诱导的间充质干细胞分泌的外泌体circNOTCH1可以通过激活NOTCH信号通路,诱导巨噬细胞M2极化来缓解糖尿病性心肌病(Diabetic cardiomyopathy,DCM)[107]
脓毒症抑制mRNA表达和促炎介质的产生,包括肿瘤坏死因子α、白细胞介素-1β、白细胞介素-6、cox-2和LPS刺激的巨噬细胞诱导的一氧化氮合酶[108]
Rg5肺部炎症抑制LPS与巨噬细胞上的toll样受体-4的结合[109]
特应性皮炎下调人角质形成细胞和巨噬细胞中NF-κB/p38MAPK/STAT1信号传导,减弱TNF-α/IFN-γ诱导的胸腺活化调节趋化因子(Thymus andactivation regulated chemokine,TARC)/CCL17的产生和LPS诱导的NO产生[110]
Rg3视网膜缺血再灌注缓解氧化应激和促进小胶质细胞/巨噬细胞M2极化[111]
人参多糖关节炎使Peyer's结淋巴细胞(Lymphocytes of Peyer's patch,PPL)分泌TNF-α,使IFN-γ的分泌增加,而上皮内淋巴细胞(Intraepithelial lymphocytes,IELs)和固有层淋巴细胞(Lamina propria lymphocytes,LPLs)所分泌的TNF-α和IFN-γ的水平均有不同程度地降低[112]
人参挥发油抗炎抑制巨噬细胞的TNF-α、IL-6和IL-1β蛋白质分泌量及IImRNA的表达水平[26]
胃癌通过作用表皮生长因子受体(Epidermal growth factor receptor,EGFR)、MAPK1、MAPK3和IL-6这几个靶点来实现治疗胃癌作用[113]
), ArticleFig(id=1322923631017341878, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=EN, label=null, caption=null, figureFileSmall=null, figureFileBig=null, tableContent=
编号药对作用机制参考文献
1人参-黄芪增加小鼠特异性免疫(脾脏淋巴细胞增殖转化率)和非特异性免疫(NK细胞杀伤活性)[143]
2人参-丹参增强T淋巴细胞对肿瘤细胞体外的杀伤能力[144]
3人参-鸡胚通过氧化低密度脂蛋白(ox-LDL)和H2O2诱导脐静脉内皮细胞(Human Umbilical Vein Endothelial Cells,HUVECs)抑制巨噬细胞存活率[139]
4人参-雷公藤调节Treg/Th17之间的平衡[145]
5人参-玛咖提高小鼠单核-巨噬细胞功能、细胞免疫功能和体液免疫功能[137]
6人参-五灵脂增加血中红细胞、白细胞数及免疫器官胸腺、脾脏、肾上腺的重量[146]
7人参-当归对环磷酞胺引起的小鼠骨髓抑制和免疫抑制均有较好的改善作用,而当参、归为1∶2的配伍比例时,促进造血功能、改善免疫功能的效果最好[147]
8人参-蒲公英人参-蒲公英配伍后可以改善免疫系统(IL-2、IL-6、TNF-α降低)相关指标的分泌[148]
), ArticleFig(id=1322923631101227959, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=CN, label=表8, caption=

人参在不同药对环境中的表达

, figureFileSmall=null, figureFileBig=null, tableContent=
编号药对作用机制参考文献
1人参-黄芪增加小鼠特异性免疫(脾脏淋巴细胞增殖转化率)和非特异性免疫(NK细胞杀伤活性)[143]
2人参-丹参增强T淋巴细胞对肿瘤细胞体外的杀伤能力[144]
3人参-鸡胚通过氧化低密度脂蛋白(ox-LDL)和H2O2诱导脐静脉内皮细胞(Human Umbilical Vein Endothelial Cells,HUVECs)抑制巨噬细胞存活率[139]
4人参-雷公藤调节Treg/Th17之间的平衡[145]
5人参-玛咖提高小鼠单核-巨噬细胞功能、细胞免疫功能和体液免疫功能[137]
6人参-五灵脂增加血中红细胞、白细胞数及免疫器官胸腺、脾脏、肾上腺的重量[146]
7人参-当归对环磷酞胺引起的小鼠骨髓抑制和免疫抑制均有较好的改善作用,而当参、归为1∶2的配伍比例时,促进造血功能、改善免疫功能的效果最好[147]
8人参-蒲公英人参-蒲公英配伍后可以改善免疫系统(IL-2、IL-6、TNF-α降低)相关指标的分泌[148]
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人参调节免疫系统疾病研究进展及质量标志物预测分析
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徐慧 1 , 冉靖 1 , 王丹 2 , 张巍 1 , 白雪媛 1
中华中医药学刊 | 国家项目点击 2025,43(5): 129-138
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中华中医药学刊 |国家项目点击 2025 , 43 (5) : 129 -138
人参调节免疫系统疾病研究进展及质量标志物预测分析
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徐慧(2001-),女,贵州铜仁人,硕士,研究方向:中药有效成分发现、生物转化及健康产品研究与开发。

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徐慧1, 冉靖1, 王丹2, 张巍1 , 白雪媛1
作者信息
  • 1.长春中医药大学东北亚中医药研究院,吉林 长春 130021
  • 2.长春金赛药业有限责任公司,吉林 长春 130021
通讯作者:
张巍(1980-),男,吉林长春人,副研究员,硕士研究生导师,博士,研究方向:中药分析新方法与新技术。E-mail:。
白雪媛(1980-),女,吉林长春人,研究员,博士研究生导师,硕士,研究方向:中药传统功效生物学机制研究及产品开发。E-mail:。
作者简介:

徐慧(2001-),女,贵州铜仁人,硕士,研究方向:中药有效成分发现、生物转化及健康产品研究与开发。

Research Progress on Renshen(Ginseng Radix et Rhizoma)Regulating Immune System Diseases and Quality Marker Prediction Analysis
Hui XU1, Jing RAN1, Dan WANG2, Wei ZHANG1 , Xueyuan BAI1
Affiliations
  • 1.Northeast Asia Institute of Traditional Chinese Medicine,Changchun University of Chinese Medicine,Changchun 130021,Jilin,China
  • 2.Changchun Jinsai Pharmaceutical Co.,Ltd,Changchun 130021,Jilin,China
出版时间: 2025-05-10 doi: 10.13193/j.issn.1673-7717.2025.05.026
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人参为五加科(Araliaceae)植物人参Panaxginseng C. A. Mey.的干燥根及根茎。主要化学成分包括皂苷、多糖、聚炔醇、挥发油、蛋白质、多肽、氨基酸等。在总结人参调节免疫功能的化学成分和药理作用的基础上,基于质量标志物(Quality marker,Q-Marker)原则从植物亲缘性,化学成分有效性,特有性和复方配伍等方面进行预测分析。大类成分以人参皂苷、多糖、蛋白质、挥发油为人参调节免疫功能的质量标志物,单一成分可选取人参皂苷Rg1、Re、Rb1、Rg3、Rh1、Rh2、Rd、CK、Ro、Rg5、人参D-葡萄糖、半乳糖、阿拉伯糖、人参炔醇作为备选物质,为其提供一定的质量控制方法参考。

人参  /  免疫调节  /  化学成分  /  药理作用  /  质量标志物  /  综述

Renshen(Ginseng Radix et Rhizoma)is the dried root and rhizome of plant Renshen(Panax ginseng C. A. Mey.). The main chemical components include saponins,polysaccharides,polyynols,volatile oils,proteins,peptides,amino acids,etc. In this paper,based on the summary of the chemical composition and pharmacological effects of Renshen(Ginseng Radix et Rhizoma)regulating immune function and the principle of quality marker(Q-Marker),the plant affinity,the effectiveness of chemical components,the specificity and the compatibility of compound formulae were predicted and analyzed. Ginsenosides,polysaccharides,proteins and volatile oils were the Q-Markers of Renshen(Ginseng Radix et Rhizoma)regulating immune function,and ginsenosides Rg1,Re,Rb1,Rg3,Rh1,Rh2,Rd,CK,Ro,Rg5,ginseng D-glucose,galactose,arabinose and ginsekyl can be selected as alternative substances for a single component,which can provide a certain quality control method reference.

Renshen(Ginseng Radix et Rhizoma)  /  immunomodulation  /  chemical composition  /  pharmacological action  /  quality markers  /  review
徐慧, 冉靖, 王丹, 张巍, 白雪媛. 人参调节免疫系统疾病研究进展及质量标志物预测分析. 中华中医药学刊, 2025 , 43 (5) : 129 -138 . DOI: 10.13193/j.issn.1673-7717.2025.05.026
Hui XU, Jing RAN, Dan WANG, Wei ZHANG, Xueyuan BAI. Research Progress on Renshen(Ginseng Radix et Rhizoma)Regulating Immune System Diseases and Quality Marker Prediction Analysis[J]. Chinese Archives of Traditional Chinese Medicine, 2025 , 43 (5) : 129 -138 . DOI: 10.13193/j.issn.1673-7717.2025.05.026
人参为五加科(Araliaceae)植物人参Panaxginseng C. A. Mey.的干燥根及根茎[1]。人参为东北地区道地药材,主要分布在吉林、黑龙江、辽宁等省份。近年来,人参作为重要原材料,经过加工处理,在市场上已经开发出普通食品、保健食品、化妆品、药品、生物制剂等5大系列1000多种产品,并且其产品需求量持续增加,市场空间广阔,发展潜力巨大[2]。免疫调节是指免疫系统根据不同的刺激和需求,调整或平衡免疫反应的过程。免疫系统的主要功能是识别和抵御入侵的病原体,但过度活跃的免疫反应可能导致自身免疫疾病或过敏反应,而免疫调节的作用就是控制和调整免疫系统的功能,以保持免疫平衡和适当的免疫反应。
人参作为一种传统中药,在许多文化中都被认为具有增强免疫功能的作用。但是目前对于人参调节免疫功能的质量标准体系有待完善。故本文通过对人参调节免疫功能起作用的化学成分,药理作用进行总结,并基于刘昌孝院士提出的QMarker理论对人参调节免疫功能的Q-Marker进行预测分析。为人参调节免疫功能的质量控制方法提供科学依据和研究思路。
现代研究表明,人参富含多种化学成分,主要包括皂苷、多糖、聚炔醇、挥发油、蛋白质、多肽、氨基酸等,本文主要针对具有调节免疫功能的皂苷类、多糖类、蛋白质类和挥发油类成分进行综合分析。
人参皂苷按其化学性质可分为:人参皂苷二醇型(A型)、人参皂苷三醇型(B型)和齐墩果酸型(C型)。现代研究表明人参皂苷Rg1、Rg3、Rb1、Rh1、Rh2、Re、Rd、CK、Ro、Rg5对免疫调节功能均有作用[3-5]。相关皂苷类成分分子式见表1,结构见图1。
人参含有的糖类成分主要有单糖、低聚糖和多糖,有一定生理活性的人参糖类成分称为人参多糖。研究表明人参多糖中免疫活性效应部位是由中性多糖和酸性多糖组成的杂多糖。中性多糖主要由半乳糖、阿拉伯糖、葡萄糖和鼠李糖组成;酸性多糖主要由葡萄糖、鼠李糖、阿拉伯糖、半乳糖、半乳糖醛酸和葡萄糖醛酸组成[19-21]。分子式见表2,结构式见图2。
目前对蛋白质的研究大多集中在提取,分离与纯化,对其化学成分的研究较少。方小雪等[23]采用高效液相色谱(High performance liquid chromatography,HPLC)测定人参蛋白的氨基酸组成和分子量发现人参蛋白由蛋白质片段组成,含有17个氨基酸。研究表明人参蛋白具有增加小鼠细胞免疫、增加免疫器官重量等作用[24]。
人参挥发油的化学成分主要包括萜类、醇类、酮类、醛类、酚类、杂环类、烷烃及其他化合物等[25],左旭[26]凭借气相色谱-质谱联用仪检测人参挥发油成分。一共检测出40种化合物,主要占比为:人参环氧炔醇(41.12%)和人参炔醇(26.90%)。
免疫调节通路非常复杂,涉及多种免疫细胞、分子和信号传导途径。目前,尚未有一个明确的数字来表示免疫调节通路的种类。但可以根据已知的免疫细胞进行大致的分类,本文通过对T淋巴细胞、B淋巴细胞、树突状细胞(Dendritic cell,DC)、自然杀伤细胞(Natural killer cell,NK)和巨噬细胞调节免疫功能进行综合分析。
T淋巴细胞负责识别和杀伤受感染的细胞。T淋巴细胞可以分为几个亚群,包括辅助T细胞和细胞毒性T细胞。目前已有多项研究表明人参中化学成分对T淋巴细胞调节免疫功能有作用。见表3。
B淋巴细胞是一种能产生抗体的淋巴细胞。当外来物质(抗原)侵入体内时,B淋巴细胞会识别并结合抗原,然后分化为浆细胞,产生大量抗体来中和并清除抗原。已有研究表明人参皂苷具有作用于B淋巴细胞进行免疫调节功能的作用。见表4。
树突状细胞是一种特殊类型的抗原呈递细胞,具有捕捉、处理、呈递抗原和激活T淋巴细胞的作用,可连接先天性和适应性免疫系统功能[71]。有研究表明人参皂苷、多糖对树突状细胞进行调节免疫系统均有作用[72-73]。见表5。
NK是人体内重要的先天免疫细胞,也是B细胞、T细胞后发现的第三类淋巴细胞,是机体固有免疫反应的重要组成成分。NK细胞主要存在于淋巴器官以及外周组织之中,对于人体内环境的平衡有着一定的积极意义[79-80]。它们可以在没有抗体和MHC的情况下识别靶细胞,并且不需要激活来杀死靶细胞,从而实现快速免疫反应。除了非特异性地杀死靶细胞外,NK细胞还释放促炎细胞因子[81]。NK细胞与多种疾病的发生、发展或治疗有关,而人参可通过多通道、多途径对NK细胞的调节延缓疾病进展。见表6。
巨噬细胞是防止外来入侵的第一道防线,活化的巨噬细胞通常分为两类,经典极化(M1型)和交替极化(M2型)巨噬细胞。M1巨噬细胞和M2巨噬细胞均与炎症反应密切相关,其中M1巨噬细胞主要参与促炎反应,M2巨噬细胞主要参与抗炎反应[86-88]。人参可通过多通道、多途径对巨噬细胞进行免疫调节。见表7。
本文根据刘昌孝[114]院士提出的中药Q-Marker进行总结综述,旨在完善中药及其复方质量标准的不足。对人参调节免疫功能的科学质量控制方法提供依据。
人参属中药是指《中华人民共和国药典》中收录的人参、红参、西洋参和三七[115]。人参种植历史约400年,但由于人参对生态环境的要求比较严格,所以世界上只有少部分区域适合生长,其道地产地并不固定,经历了重大的变迁。产区从太行山-燕山-长白山一线的区域逐渐向北缩减,如今只剩长白山一小块区域[116-117]。同时研究表明,利用表达序列标签[(Expressed sequence tag,EST)-SSR]引物用于人参、西洋参和三七进行种间鉴定,可以为人参属物种的系统进化和亲缘关系研究提供足够信息,为人参属植物种间鉴定提供了一定技术手段[118]。
人参含有许多化学成分,而一种化学成分又存在于不同的中药中,因此,对比人参基原的成分分析及其特有成分,从而反映出人参的特有性,可作为预测人参调节免疫功能Q-Marker的依据。人参化学成分包括皂苷、多糖、聚炔醇、挥发油、蛋白质、多肽、氨基酸、维生素、有机酸、微量元素等。刘永利[119]等人利用液相色谱-质谱联用方法分别对人参、西洋参、三七药材进行测定,得出3种药材中共有皂苷类成分比例各有特点,特别是Rg1、Re与Rb1三者的比例关系。因此人参中共有成分的比例(人参皂苷Rg1、Re、Rb1)组合可作为其潜在的QMarker。
中药性味归经是中药的基本属性,是中医临床用药配伍的重要依据,由四气、五味、归经、毒性、升降浮沉等构成[120]。集中概括了中药用药规律,与中药药效密切相关,可作为预测Q-Marker的依据之一。
中药化学成分与中药药性密切相关,人参药性为甘、微苦,微温,归脾、肺、心、肾经[121]。“甘”为中药五味之一,具有能补、能缓、能和等功效,主要与糖类、蛋白质、氨基酸等成分相关[122-123]。现代研究表明,甘味药具有调节机能、补充机体不足、增强机体抗病能力以及杀菌等方面的作用[124]。人参皂苷、氨基酸、维生素、多肽等,这些主要化学成分是人参苦味物质的主要来源;李新等研究表明,苦味药有的能调节机体功能活动,有的对机体的非特异性或特异性免疫功能有调节作用[125-126]。因此人参多糖、人参皂苷、人参蛋白质可作为人参调节免疫的Q-Marker之一。
人参首见于《神农本草经》,被列为上品,称其“主补五脏,安精神,安魂魄,止惊悸,除邪气,明目,开心益智,久服轻身延年”,现代药理学研究表明,其具有增强记忆力、抗肿瘤、保护心血管、提高免疫力等作用。当机体免疫系统发生紊乱时,便会引发各种疾病,如炎症、肿瘤、糖尿病、肝肾等[127]。
目前很多研究报道了人参皂苷具有调节免疫功能的作用,其主要成分有人参皂苷(Rg1,Rg3,Rb1,Rh1,Rh2,Re,Rd,CK、Ro、Rg5)和人参多糖等,此类成分在体内和体外的多种研究中均表现出良好的免疫调节能力。体外实验中,人参多糖主要通过激活巨噬细胞、树突状细胞和补体系统发挥免疫调节功能;体内实验中,人参多糖可以增加免疫器官指数,刺激淋巴细胞,调节多种免疫细胞和免疫介质,维持机体内环境的稳定人参多糖可应用于多种免疫性疾病的治疗[128-129]。焦丽丽[130]等研究发现人参低聚糖(由D-葡萄糖组成)可以抑制体内肿瘤生长,显著增加血清肿瘤坏死因子-α水平、脾脏淋巴细胞、自然杀伤细胞活性、吞噬功能和巨噬细胞分泌一氧化氮。有学者[131]从人参浆果中分离得到了半乳糖和阿拉伯糖,具有很强的免疫增强活性。当前已从人参中分离得到多种蛋白质类化合物[132-133],现代研究表明:人参蛋白具有增强小鼠细胞免疫、免疫器官重量、巨噬细胞免疫活性,促进释放免疫因子、耐缺氧、抗疲劳、抗氧化等作用[24,133]。对于其免疫调节机理,还有待进一步研究。邵琦[134]等研究发现人参炔醇可重塑巨噬细胞表型和功能,从而间接改变乳腺癌细胞生物学行为。
因此可将人参皂苷Rg1、Rg3、Rb1、Rh1、Rh2、Re、Rd、CK、Ro、Rg5、人参D-葡萄糖、半乳糖、阿拉伯糖、人参蛋白质、人参炔醇作为Q-Marker的备选。
药对是中医临床用药中常见的一种配伍形式,达到协同增效或减毒等作用。药对,即对药,是中药配伍中相对固定的两味药的配伍形式,药对的组成虽然简单,但两药可以相互依赖、相互制约,合理应用或可以起到协同作用或可减轻不良反应,体现出了中药配伍的基本特点,在中医药领域已发挥重要的作用。
已有多项研究表明人参药对配伍对免疫调节有良好作用。其中人参-黄芪,人参-鸡胚,人参-玛咖,人参-当归等配伍具有补中益气之功效,与雷公藤配伍则有抗炎作用[135-140]。周娅红[141]等研究发现,人参总皂苷对免疫低下小鼠具有促进作用,具有补气功能。郭校妍[142]等综述了人参皂苷Rb1,Rg1,Rg3等皂苷类成分具有抗炎作用。
现代研究表明,人参配伍丹参、鸡胚、雷公藤、玛咖是通过调节T淋巴细胞和巨噬细胞来调节免疫系统;配伍蒲公英是通过调节IL-2、IL-6、TNF-α等免疫因子来调节免疫系统;配伍五灵脂,当归通过调节胸腺、脾脏等免疫器官来调节免疫系统。具体作用机制如表。因此可将上述化学成分作为人参调节免疫系统的Q-Marker。见表8。
中药复方配伍是指在中医药理论指导下使用单味中药或多味中药结合而形成的方剂,通过运用特殊的方剂配伍环境而达到特定的疗效,以达到治疗不同疾病的目的。人参临床上常与其他药物配伍发挥药效,因此从复方配伍环境入手确定其Q-Marker也是很好的途径。四君子汤是十分重要的益气补血中药,其组成包括人参、白术、茯苓、炙甘草四味中药,其主要化学成分是皂苷、多糖类、黄酮类及其他成分,方中人参甘温益气,既可大补脾胃之气,又可补益肺气,为君。诸药合用,主治脾胃气虚证,具有提高机体免疫力等药理作用,已有研究报道,人参总皂苷通过参与机体免疫调节作用的细胞因子水平降低治疗脾虚,因此可以把人参皂苷作为其Q-Marker[149-150]。
人参用药历史悠久,具有广泛的药理作用。现代对于人参调节免疫功能研究发现,皂苷类、多糖类成分发挥作用居多,此外人参蛋白质、挥发油也有一定作用。由于人参调节免疫功能是利用其“多成分,多靶点,多途径”的药理学特征,现行的质量控制方法存在一定的缺陷,无法达到全面评价中药质量的效果。因此建立一个更为全面、科学的质量控制标准尤为重要。本文归纳了人参调节免疫功能的化学成分和药理作用机制,并基于Q-Marker理论,从植物亲缘性、化学成分特有性、有效性以及复方配伍等多个方面进行分析,对人参调节免疫功能的Q-Marker展开预测,初步认为人参皂苷、多糖、蛋白质、挥发油等成分可作为人参调节免疫系统的Q-Marker,单一成分可选取人参皂苷Rg1、Re、Rb1、Rg3、Rh1、Rh2、Rd、CK、Ro、Rg5、人参D-葡萄糖、半乳糖、阿拉伯糖、人参炔醇等成分作为其QMarker,为探索人参调节免疫功能的质量控制体系奠定了基础。
  • 国家自然科学基金联合基金重点支持项目(U19A2013)
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2025年第43卷第5期
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doi: 10.13193/j.issn.1673-7717.2025.05.026
  • 首发时间:2026-10-30
  • 出版时间:2025-05-10
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国家自然科学基金联合基金重点支持项目(U19A2013)
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    1.长春中医药大学东北亚中医药研究院,吉林 长春 130021
    2.长春金赛药业有限责任公司,吉林 长春 130021

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张巍(1980-),男,吉林长春人,副研究员,硕士研究生导师,博士,研究方向:中药分析新方法与新技术。E-mail:。
白雪媛(1980-),女,吉林长春人,研究员,博士研究生导师,硕士,研究方向:中药传统功效生物学机制研究及产品开发。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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