Article(id=1317115232573576011, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317115025307845060, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2026.05.001, 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=1791954342263, onlineDateStr=2026-10-14, pubDate=1778342400000, pubDateStr=2026-05-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1791954342263, onlineIssueDateStr=2026-10-14, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1791954342263, creator=13701087609, updateTime=1791954342263, updator=13701087609, issue=Issue{id=1317115025307845060, tenantId=1146029695717560320, journalId=1255847919539208197, year='2026', volume='44', issue='5', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1778342400000', pubDateStr='2026-05-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1791954292847, creator='13701087609', updateTime=1791958713604, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1317133567340171275, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317115025307845060, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1317133567340171276, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317115025307845060, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1, endPage=6, ext={EN=ArticleExt(id=1317115232808457036, articleId=1317115232573576011, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Exploring the Effect of Wendan Decoction on the Inflammatory State of Obesity with Phlegm-Dampness Syndrome Based on M1 Polarization of Islet Macrophages, columnId=1256183423710970242, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=New Opinion of Ph.D. Supervisor, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the relationship between the inflammatory state of obesity with phlegm-dampness syndrome and the M1 polarization of islet macrophages, as well as the intervention mechanism of Wendan Decoction.
Methods Forty-five SD rats were randomly divided into a blank group and a modeling group. The modeling group was fed a high-fat diet for 8 weeks to establish an obesity with phlegm-dampness syndrome model. Twenty obese rats were then selected and divided into a model group, a Xuezhikang group, and low-/high-dose Wendan Decoction groups (5 rats each). The blank group (normal group) comprised 5 rats. Each treatment group received corresponding doses via gavage for 6 weeks, while the model and normal groups received equal volumes of distilled water. Body weight, Lee’s index, and lipid levels were measured. ELISA was used to determine pro-inflammatory cytokines (TNF-α, IL-6, IFN-γ) and fasting insulin (FINS) in islet tissue. HE staining and immunohistochemistry were employed to observe islet histopathology and the expression of macrophage marker CD68 (Cluster of Differentiation 68), M1 activation marker CD86 (Cluster of Differentiation 86), and iNOS (inducible nitric oxide synthase) . Western blot was used to detect CD68, CD86, and iNOS protein expression.
Results After successful modeling, pathological improvements were observed in all treatment groups. Compared with the normal group, the model group showed significant changed in body weight, Lee’s index, lipid levels (elevated TG and LDL-C, decreased HDL-C) (P<0.001 or P<0.01), FINS, HOMA-IR, and TNF-α/IL-6 secretion (P<0.05、P<0.01 or P<0.001) . Compared with the model group, all treatment groups exhibited significant reductions in body weight, obesity rate, TG, FINS, HOMA-IR, and TNF-α/IL-6 secretion (P<0.01、P<0.05 or P<0.001). The high-dose Wendan Decoction group showed significant decreases in Lee’s index and LDL-C (P<0.01 or P<0.05) . Histopathological and immunohistochemical analyses showed that the infiltration of CD68, CD86, and iNOS positive cells in the islet interstitium was significantly increased in the model group (P<0.05) ; the integrity of islet tissue was improved in each treatment group, with significantly reduced infiltration of CD68, CD86, and iNOS positive cells (P<0.05 or P<0.01) . Among them, only a small number of positive cells were occasionally observed in the low-/high-dose Wendan Decoction groups, and the number of positive cells was relatively fewer in the Xuezhikang group. Western blot (WB) assay revealed that compared with the normal group, the protein expression levels of CD68, CD86, and iNOS in the islets were significantly elevated in the model group (P<0.000 1) ; compared with the model group, the expression of CD86 and iNOS proteins was significantly reduced in the low-dose Wendan Decoction group (P<0.05 or P<0.001), while the expression of CD68, CD86, and iNOS proteins was significantly decreased in both the high-dose Wendan Decoction group and the Xuezhikang group (P<0.001). The high-dose Wendan Decoction group outperformed the Xuezhikang group in lowering Lee’s index and CD68 protein expression (P<0.05 or P<0.001) .
Conclusion The inflammatory state of obesity with phlegm-dampness syndrome is closely associated with M1 polarization of islet macrophages (manifested as abnormal expression of CD68+, CD86+, and iNOS+) . Wendan Decoction can significantly improve the inflammatory state of obesity with phlegm-dampness syndrome by regulating M1 polarization of islet macrophages.
, authors=Songren YU
1, 2, Jialing XU
3, Zhiyong LIU
1, Guoshuang ZHU
1, Youbao ZHONG
1, Nannan SONG
1, Lebin FU
3, Jie ZHANG
1, 2, Delin ZHANG
4, authorsList=Songren YU, Jialing XU, Zhiyong LIU, Guoshuang ZHU, Youbao ZHONG, Nannan SONG, Lebin FU, Jie ZHANG, Delin ZHANG, authorCompany=null, correspAuthors=Jie ZHANG, Delin ZHANG, 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=1317115233072698189, articleId=1317115232573576011, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=基于胰岛巨噬细胞M1极化探讨温胆汤对肥胖痰湿证炎症状态的影响, columnId=1256183426563096985, journalTitle=中华中医药学刊, columnName=博士导师新论, runingTitle=null, highlight=null, articleAbstract=
目的 探讨肥胖痰湿证炎症状态与胰岛经典活化巨噬细胞（Classically activated macrophage，M1）极化的关系，以及温胆汤的干预机制。
方法 将45只斯泼累格·多雷（Sprague-Dawley，SD）大鼠随机分为空白组、造模组。造模组喂养高脂饲料8周建立肥胖痰湿证模型后，筛选出20只肥胖大鼠分为模型组、血脂康组、温胆汤低剂量组、温胆汤高剂量组，每组5只；正常组选用空白组大鼠5只。各给药组按相应剂量灌胃6周，模型组和正常组给予等体积蒸馏水。检测体质量、Lee＇s指数、血脂水平，采用酶联免疫吸附测定法（Enzyme-linked immunosorbent assay，ELISA）测定胰岛组织促炎因子肿瘤坏死因子-α（Tumor necrosis factor-alpha，TNF-α）、白细胞介素-6（Interleukin-6，IL-6）、干扰素-γ（Interferon-gamma，IFN-γ）和空腹胰岛素（Fasting insulin，FINS）水平，苏木精-伊红染色法（hematoxylin-eosin staining，HE）和免疫组化法（Immunohistochemistry，IHC）观察胰岛组织病理改变和巨噬细胞泛标志物CD68、M1活性标志物CD86和诱导型一氧化氮合酶（Inducible nitric oxide synthase，iNOS）表达，蛋白质免疫印迹法（Western blot，WB）检测CD68、CD86和iNOS蛋白含量。
结果 造模成功后，给药各组痰湿一般病理状态表现改善明显；与正常组比较，模型组体质量、Lee＇s指数、血脂水平［甘油三酯（Triglycerides，TG）、低密度脂蛋白胆固醇（Low-density lipoprotein cholesterol，LDL-C）和高密度脂蛋白胆固醇（High-density lipoprotein cholesterol，HDL-C）］显著改变（P<0.001或P<0.01），FINS、胰岛素抵抗稳态模型评估（Homeostatic model assessment for insulin resistance，HOMA-IR）及胰岛组织TNF-α、IL-6分泌显著增加（P<0.05、P<0.01或P<0.001）；与模型组比较，各给药组体质量、肥胖率、血脂水平（TG）、FINS、HOMA-IR及胰岛组织促炎因子（TNF-α、IL-6）分泌均显著降低（P<0.01，P<0.05或P<0.001），温胆汤高剂量组Lee＇s指数、LDL-C显著下降（P<0.01或P<0.05）。组织病理及IHC分析显示，模型组胰岛间质内CD68、CD86及iNOS阳性细胞浸润显著增多（P<0.05）；各用药组胰岛组织完整性改善，CD68、CD86及iNOS阳性细胞浸润显著降低（P<0.05或P<0.01），其中温胆汤低/高剂量组偶见少量阳性细胞，血脂康组阳性细胞数量较少。WB检测显示，与正常组比较，模型组胰岛CD68、CD86及iNOS蛋白表达水平显著升高（P<0.000 1）；与模型组比较，温胆汤低剂量组CD86及iNOS蛋白表达显著降低（P<0.05或P<0.01），高剂量组及血脂康组CD68、CD86及iNOS蛋白表达均显著降低（P<0.001）。温胆汤高剂量组在Lee＇s指数和CD68蛋白表达方面优于血脂康组（P<0.05或P<0.001）。
结论 肥胖痰湿证炎症状态与胰岛巨噬细胞M1极化（CD68+、CD86+和iNOS+异常表达）密切相关，温胆汤通过调控胰岛巨噬细胞M1极化可显著改善肥胖痰湿证的炎症状态。
, authors=喻松仁
1, 2, 徐佳玲
3, 刘志勇
1, 朱国双
1, 钟友宝
1, 宋楠楠
1, 傅乐斌
3, 张洁
1, 2, 章德林
4, authorsList=喻松仁, 徐佳玲, 刘志勇, 朱国双, 钟友宝, 宋楠楠, 傅乐斌, 张洁, 章德林, authorCompany=null, correspAuthors=张洁, 章德林, authorNote=
喻松仁（1976-），男，江西九江人，教授，博士研究生导师，博士，研究方向：中医证的本质。
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1. Experimental Animal Science and Technology Center, Jiangxi University of Chinese Medicine, Nanchang 330004, Jiangxi, China
2. Jiangxi Provincial Key Laboratory of Pharmacodynamic Material Basis of Traditional Chinese Medicine, Jiangxi University of Chinese Medicine, Nanchang 330004, Jiangxi, China, bio=null, bioImg=null, bioContent=null, aboutCorrespAuthor=null), CN=AuthorExt(id=1319630377245848236, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1317115232573576011, authorId=1319630377086464680, language=CN, stringName=喻松仁, firstName=null, middleName=null, lastName=null, prefix=null, suffix=null, authorComment=null, nameInitials=null, affiliation=null, department=null, xref=
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1．江西中医药大学实验动物科技中心，江西 南昌 330004
2．江西中医药大学中药药效物质基础江西省重点实验室，江西 南昌 330004, bio={"content":"
喻松仁（1976-），男，江西九江人，教授，博士研究生导师，博士，研究方向：中医证的本质。
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喻松仁（1976-），男，江西九江人，教授，博士研究生导师，博士，研究方向：中医证的本质。
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3. Graduate School, Jiangxi University of Chinese Medicine, Nanchang 330004, Jiangxi, China, bio=null, bioImg=null, bioContent=null, aboutCorrespAuthor=null), CN=AuthorExt(id=1319630377442980529, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1317115232573576011, authorId=1319630377308762798, language=CN, stringName=徐佳玲, firstName=null, middleName=null, lastName=null, prefix=null, suffix=null, authorComment=null, nameInitials=null, affiliation=null, department=null, xref=
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LZ205, a newly synthesized flavonoid compound, exerts anti-inflammatory effect by inhibiting M1 macrophage polarization through regulating PI3K/AKT/mTOR signaling pathway［J］. Exp Cell Res, 2018, 364 (1) : 84-94., articleTitle=null, refAbstract=null), Reference(id=1319630382958490351, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1317115232573576011, doi=null, pmid=null, pmcid=null, year=null, volume=null, issue=null, pageStart=null, pageEnd=null, url=null, language=null, rfNumber=［9］, rfOrder=8, authorNames=null, journalName=null, refType=null, unstructuredReference=PAN D, LI G, JIANG C L, et al. Regulatory mechanisms of macrophage polarization in adipose tissue［J］. 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