Article(id=1317115018269806697, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317114999827452826, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2026.06.006, 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=1791954291169, onlineDateStr=2026-10-14, pubDate=1781020800000, pubDateStr=2026-06-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1791954291169, onlineIssueDateStr=2026-10-14, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1791954291169, creator=13701087609, updateTime=1791954291169, updator=13701087609, issue=Issue{id=1317114999827452826, tenantId=1146029695717560320, journalId=1255847919539208197, year='2026', volume='44', issue='6', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1781020800000', pubDateStr='2026-06-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1791954286772, creator='13701087609', updateTime=1791958677365, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1317133415753831385, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317114999827452826, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1317133415753831386, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317114999827452826, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=32, endPage=35, ext={EN=ArticleExt(id=1317115018466938986, articleId=1317115018269806697, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Astragalus Polysaccharide Inhibited Progression of Peritoneal Dialysis-Related Peritoneal Fibrosis by Counteracting Epithelial-Mesenchymal Transition and Regulating M2 Macrophage Polarization, columnId=1256183361521967297, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Target on National Project, runingTitle=null, highlight=null, articleAbstract=
Objective

To investigate the intervention effects of Astragalus polysaccharide on peritoneal fibrosis related to peritoneal dialysis in mice and its possible mechanisms.

Methods

Male C57BL/6 mice were randomly divided into a blank control group (Control), a model group (Model), a low-dose group of Astragalus polysaccharide (APS 100 mg/kg) and a high-dose group of Astragalus Polysaccharide (APS 200 mg/kg), with 10 mice in each group. A mouse model of peritoneal fibrosis was established using high-glucose peritoneal dialysis fluid, and the treatment was administered daily for 28 days. After the final treatment, peritoneal function (glucose transport and urea nitrogen levels) was assessed. Hematoxylin-eosin staining (HE) and Masson staining were performed to observe the pathological changes, fibrosis and peritoneal thickness. Western blot analysis was conducted to detect the expressions of epithelial-mesenchymal transition (EMT) related proteins in peritoneal tissue. The immunohistochemistry and flow cytometry methods were used to assess the expressions of macrophage polarization-related proteins in peritoneal tissue.

Results

Compared to the Control group, the Model group showed significant increases in peritoneal thickness and collagen fiber deposition, elevated glucose transport and higher urea nitrogen levels. The expressions of EMT-related proteins[α-smooth muscle actin (α-SMA), collagen Ⅲ, fibronectin)]significantly increased, while E-cadherin protein expression significantly decreased, and M2 macrophage markers[Arginase-1 (Arg-1), CD163]were significantly elevated. In comparison to the Model group, the treatment with Astragalus polysaccharide led to significant improvements in the above indicators, with the high-dose group showing better effects than the low-dose group. After the clearance of macrophages, the inhibitory effect of Astragalus polysaccharide on the peritoneal fibrosis was weakened.

Conclusion

Astragalus polysaccharide inhibits the peritoneal fibrosis in mice by suppressing epithelial-mesenchymal transition and regulating M2 macrophage polarization.

, authors=Junyi ZHAO1, 2, Mengya WANG3, Mengyun YUAN4, Wen ZHOU1, authorsList=Junyi ZHAO, Mengya WANG, Mengyun YUAN, Wen ZHOU, authorCompany=null, correspAuthors=Wen ZHOU, 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=1317115018743763051, articleId=1317115018269806697, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=黄芪多糖通过抑制上皮-间充质转化及M2巨噬细胞极化改善腹膜透析相关腹膜纤维化进展, columnId=1256183362172142382, journalTitle=中华中医药学刊, columnName=国家项目点击, runingTitle=null, highlight=null, articleAbstract=
目的

探讨黄芪多糖对小鼠腹膜透析相关腹膜纤维化的干预作用及其可能机制。

方法

雄性C57BL/6小鼠随机分为空白对照组(Control组)、模型组(Model组)、黄芪多糖低剂量组(Astragalus Polysaccharide,APS 100 mg/kg)和黄芪多糖高剂量组(APS 200 mg/kg),每组10只。构建高糖腹膜透析液诱导的小鼠腹膜纤维化模型,连续28天给药。末次给药后,检测小鼠腹膜功能(葡萄糖转运量、尿素氮水平);苏木素-伊红(Hematoxylin and Eosin,HE)和马松(Masson)染色观察腹膜组织病理学变化、纤维化情况以及腹膜厚度;Western bolt实验检测腹膜组织中上皮-间充质转化(Epithelial-Mesenchymal Transition,EMT)相关蛋白表达;免疫组化染色和流式细胞术检测腹膜组织中巨噬细胞极化相关蛋白表达。利用巨噬细胞清除剂氯膦酸盐脂质体(Clodronate liposomes,CL)来检测黄芪多糖阻止腹膜纤维化进展是否依赖于巨噬细胞的作用。

结果

与Control组相比,Model组小鼠腹膜厚度和胶原纤维沉积显著增加,葡萄糖转运量显著提升,尿素氮水平显著升高;EMT相关蛋白[α-平滑肌动蛋白(Alpha-Smooth Muscle Actin,α-SMA)、Ⅲ型胶原蛋白(Collagen Ⅲ)、纤维连接蛋白(Fibronectin)]表达显著增加,而上皮钙黏蛋白(E-cadherin)蛋白表达显著降低,M2型巨噬细胞标志物[精氨酸酶-1(Arginase 1,Arg-1)、CD163]表达显著增加。与Model组比较,黄芪多糖给药组的小鼠上述指标均显著改善,且高剂量组效果优于低剂量组。巨噬细胞清除后,黄芪多糖对小鼠腹膜纤维化的抑制作用减弱。

结论

黄芪多糖通过抑制上皮-间充质转化并调节巨噬细胞M2极化抑制小鼠腹膜纤维化。

, authors=赵君谊1, 2, 王梦亚3, 袁梦云4, 周雯1, authorsList=赵君谊, 王梦亚, 袁梦云, 周雯, authorCompany=null, correspAuthors=周雯, authorNote=

赵君谊(1990-),女,江苏镇江人,讲师,博士,研究方向:中医文献与中医药改善腹透效能。

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周雯(1988-),女,江苏南京人,讲师,博士,研究方向:脾藏象的现代研究。E-mail:。
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黄芪多糖通过抑制上皮-间充质转化及M2巨噬细胞极化改善腹膜透析相关腹膜纤维化进展
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赵君谊 1, 2 , 王梦亚 3 , 袁梦云 4 , 周雯 1
中华中医药学刊 | 国家项目点击 2026,44(6): 32-35
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中华中医药学刊 |国家项目点击 2026 , 44 (6) : 32 -35
黄芪多糖通过抑制上皮-间充质转化及M2巨噬细胞极化改善腹膜透析相关腹膜纤维化进展
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赵君谊1, 2, 王梦亚3, 袁梦云4, 周雯1
作者信息
  • 1.南京中医药大学,江苏 南京 210023
  • 2.江苏省中医流派研究院,江苏 南京 210023
  • 3.南京医科大学第四附属医院,江苏 南京 210029
  • 4.南京中医药大学附属医院江苏省中医院,江苏 南京 210029
通讯作者:
周雯(1988-),女,江苏南京人,讲师,博士,研究方向:脾藏象的现代研究。E-mail:。
作者简介:

赵君谊(1990-),女,江苏镇江人,讲师,博士,研究方向:中医文献与中医药改善腹透效能。

Astragalus Polysaccharide Inhibited Progression of Peritoneal Dialysis-Related Peritoneal Fibrosis by Counteracting Epithelial-Mesenchymal Transition and Regulating M2 Macrophage Polarization
Junyi ZHAO1, 2, Mengya WANG3, Mengyun YUAN4, Wen ZHOU1
Affiliations
  • 1.Nanjing University of Chinese Medicine, Nanjing 210023, Jiangsu, China
  • 2.Jiangsu Provincial Research Institute of Chinese Medicine Schools, Nanjing 210023, Jiangsu, China
  • 3.The Fourth Affiliated Hospital, Nanjing Medical University, Nanjing 210029, Jiangsu, China
  • 4.Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, Jiangsu, China
出版时间: 2026-06-10 doi: 10.13193/j.issn.1673-7717.2026.06.006
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目的

探讨黄芪多糖对小鼠腹膜透析相关腹膜纤维化的干预作用及其可能机制。

方法

雄性C57BL/6小鼠随机分为空白对照组(Control组)、模型组(Model组)、黄芪多糖低剂量组(Astragalus Polysaccharide,APS 100 mg/kg)和黄芪多糖高剂量组(APS 200 mg/kg),每组10只。构建高糖腹膜透析液诱导的小鼠腹膜纤维化模型,连续28天给药。末次给药后,检测小鼠腹膜功能(葡萄糖转运量、尿素氮水平);苏木素-伊红(Hematoxylin and Eosin,HE)和马松(Masson)染色观察腹膜组织病理学变化、纤维化情况以及腹膜厚度;Western bolt实验检测腹膜组织中上皮-间充质转化(Epithelial-Mesenchymal Transition,EMT)相关蛋白表达;免疫组化染色和流式细胞术检测腹膜组织中巨噬细胞极化相关蛋白表达。利用巨噬细胞清除剂氯膦酸盐脂质体(Clodronate liposomes,CL)来检测黄芪多糖阻止腹膜纤维化进展是否依赖于巨噬细胞的作用。

结果

与Control组相比,Model组小鼠腹膜厚度和胶原纤维沉积显著增加,葡萄糖转运量显著提升,尿素氮水平显著升高;EMT相关蛋白[α-平滑肌动蛋白(Alpha-Smooth Muscle Actin,α-SMA)、Ⅲ型胶原蛋白(Collagen Ⅲ)、纤维连接蛋白(Fibronectin)]表达显著增加,而上皮钙黏蛋白(E-cadherin)蛋白表达显著降低,M2型巨噬细胞标志物[精氨酸酶-1(Arginase 1,Arg-1)、CD163]表达显著增加。与Model组比较,黄芪多糖给药组的小鼠上述指标均显著改善,且高剂量组效果优于低剂量组。巨噬细胞清除后,黄芪多糖对小鼠腹膜纤维化的抑制作用减弱。

结论

黄芪多糖通过抑制上皮-间充质转化并调节巨噬细胞M2极化抑制小鼠腹膜纤维化。

黄芪多糖  /  腹膜纤维化  /  上皮-间充质转化  /  巨噬细胞
Objective

To investigate the intervention effects of Astragalus polysaccharide on peritoneal fibrosis related to peritoneal dialysis in mice and its possible mechanisms.

Methods

Male C57BL/6 mice were randomly divided into a blank control group (Control), a model group (Model), a low-dose group of Astragalus polysaccharide (APS 100 mg/kg) and a high-dose group of Astragalus Polysaccharide (APS 200 mg/kg), with 10 mice in each group. A mouse model of peritoneal fibrosis was established using high-glucose peritoneal dialysis fluid, and the treatment was administered daily for 28 days. After the final treatment, peritoneal function (glucose transport and urea nitrogen levels) was assessed. Hematoxylin-eosin staining (HE) and Masson staining were performed to observe the pathological changes, fibrosis and peritoneal thickness. Western blot analysis was conducted to detect the expressions of epithelial-mesenchymal transition (EMT) related proteins in peritoneal tissue. The immunohistochemistry and flow cytometry methods were used to assess the expressions of macrophage polarization-related proteins in peritoneal tissue.

Results

Compared to the Control group, the Model group showed significant increases in peritoneal thickness and collagen fiber deposition, elevated glucose transport and higher urea nitrogen levels. The expressions of EMT-related proteins[α-smooth muscle actin (α-SMA), collagen Ⅲ, fibronectin)]significantly increased, while E-cadherin protein expression significantly decreased, and M2 macrophage markers[Arginase-1 (Arg-1), CD163]were significantly elevated. In comparison to the Model group, the treatment with Astragalus polysaccharide led to significant improvements in the above indicators, with the high-dose group showing better effects than the low-dose group. After the clearance of macrophages, the inhibitory effect of Astragalus polysaccharide on the peritoneal fibrosis was weakened.

Conclusion

Astragalus polysaccharide inhibits the peritoneal fibrosis in mice by suppressing epithelial-mesenchymal transition and regulating M2 macrophage polarization.

Astragalus polysaccharide  /  peritoneal fibrosis  /  epithelial-mesenchymal transformation  /  macrophage
赵君谊, 王梦亚, 袁梦云, 周雯. 黄芪多糖通过抑制上皮-间充质转化及M2巨噬细胞极化改善腹膜透析相关腹膜纤维化进展. 中华中医药学刊, 2026 , 44 (6) : 32 -35 . DOI: 10.13193/j.issn.1673-7717.2026.06.006
Junyi ZHAO, Mengya WANG, Mengyun YUAN, Wen ZHOU. Astragalus Polysaccharide Inhibited Progression of Peritoneal Dialysis-Related Peritoneal Fibrosis by Counteracting Epithelial-Mesenchymal Transition and Regulating M2 Macrophage Polarization[J]. Chinese Archives of Traditional Chinese Medicine, 2026 , 44 (6) : 32 -35 . DOI: 10.13193/j.issn.1673-7717.2026.06.006
  • 国家自然科学基金青年科学基金项目(82104703)
  • 江苏高校哲学社会科学研究一般项目(2023SJYB0328)
  • 江苏省中医流派研究院开放课题一般项目(JSZYLP2024022)
  • 南京中医药大学教育发展基金会项目(LLX202201)
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2026年第44卷第6期
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doi: 10.13193/j.issn.1673-7717.2026.06.006
  • 首发时间:2026-10-14
  • 出版时间:2026-06-10
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基金
国家自然科学基金青年科学基金项目(82104703)
江苏高校哲学社会科学研究一般项目(2023SJYB0328)
江苏省中医流派研究院开放课题一般项目(JSZYLP2024022)
南京中医药大学教育发展基金会项目(LLX202201)
作者信息
    1.南京中医药大学,江苏 南京 210023
    2.江苏省中医流派研究院,江苏 南京 210023
    3.南京医科大学第四附属医院,江苏 南京 210029
    4.南京中医药大学附属医院江苏省中医院,江苏 南京 210029

通讯作者:

周雯(1988-),女,江苏南京人,讲师,博士,研究方向:脾藏象的现代研究。E-mail:。
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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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