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 XU
1, Jing RAN
1, Dan WANG
2, Wei ZHANG
1, Xueyuan BAI
1, 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=
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:
23165956@qq.com。
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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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人参调节免疫功能的主要皂苷类成分结构, figureFileSmall=0XRUBnTnBpz1/Iq4sOLg0Q==, figureFileBig=/YikoEH7QPrrU4ln3N+Cvw==, tableContent=null), ArticleFig(id=1322923627762561954, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=EN, label=null, caption=null, figureFileSmall=JG7pOik+7gzCvWk5XfVzOQ==, figureFileBig=g7q4owifBRk161S8M069Jg==, tableContent=null), ArticleFig(id=1322923627833865123, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923613556454234, language=CN, label=图2, caption=
人参调节免疫功能的主要多糖类成分结构式, figureFileSmall=JG7pOik+7gzCvWk5XfVzOQ==, figureFileBig=g7q4owifBRk161S8M069Jg==, tableContent=null), ArticleFig(id=1322923627896779684, 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 |
|---|
| 1 | Rg1 | C42H72O14 | [6] |
| 2 | Rg3 | C42H72O13 | [7-8] |
| 3 | Rb1 | C54H92O23 | [9-10] |
| 4 | Rh1 | C36H62O9 | [11] |
| 5 | Rh2 | C36H62O8 | [12-13] |
| 6 | Re | C48H82O18 | [14-15] |
| 7 | Rd | C48H82O18 | [4] |
| 8 | CK | C36H62O8 | [16] |
| 9 | Ro | C48H76O19 | [17] |
| 10 | Rg5 | C42H70O12 | [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 |
|---|
| 1 | Rg1 | C42H72O14 | [6] |
| 2 | Rg3 | C42H72O13 | [7-8] |
| 3 | Rb1 | C54H92O23 | [9-10] |
| 4 | Rh1 | C36H62O9 | [11] |
| 5 | Rh2 | C36H62O8 | [12-13] |
| 6 | Re | C48H82O18 | [14-15] |
| 7 | Rd | C48H82O18 | [4] |
| 8 | CK | C36H62O8 | [16] |
| 9 | Ro | C48H76O19 | [17] |
| 10 | Rg5 | C42H70O12 | [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] |
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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] |
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人参在不同药对环境中的表达
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| 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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