Article(id=1291404583159452015, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404554201985968, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.06.018, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1730044800000, receivedDateStr=2024-10-28, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824445761, onlineDateStr=2026-08-04, pubDate=1743091200000, pubDateStr=2025-03-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824445761, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824445761, creator=13701087609, updateTime=1785824445761, updator=13701087609, issue=Issue{id=1291404554201985968, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='6', pageStart='751', pageEnd='900', issueExtLink='null', onlineDate='null', pubDate='1743091200000', pubDateStr='2025-03-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824438858, creator='13701087609', updateTime=1785824438858, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=846, endPage=851, ext={EN=ArticleExt(id=1291404583608242544, articleId=1291404583159452015, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Effects of sinomenine on collagen-induced arthritis rats
via regulating macrophage polarization, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the possible mechanism of action of sinomenine (Sin) in the treatment of collagen-induced arthritis (CIA) rats by regulating macrophage polarization.
Methods Wistar rats were randomly divided into control group (normal diet and care), model group (CIA model was established with bovine type Ⅱ collagen at the tail), experimental-L, -M, -H groups (all on the basis of the model group, 40, 80 and 160 mg·kg-1 Sin by gavage respectively), inh-NC group and inh-miR-885-5p group[on the basis of the experimental-H group, the two groups were injected with a negative control of microRNA-885-5p (miR-885-5p) and miR-885-5p inhibitor in the tail vein, respectively)], for four weeks, with 10 rats in each group. The arthritis index (AI) and plantar swelling of rats in each group were statistically analyzed. The pathological conditions of the synovial tissue of the ankle joint were observed by hematoxylin-eosin staining. Real-time fluorescent quantitative polymerase chain reaction was performed to examine the relative expression level of miR-885-5p in rat synovial tissue. Western blot was carried out to detect the expression of related proteins in the synovial tissue of rats. Enzyme-linked immunosorbent assay was used to detect the level of serum inflammatory factors. Terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) was used to detect the apoptosis of rat synovial cells.
Results The AI scores of the control group, model group and experimental-H group were 0, (7.20±1.38) and (5.50±1.10) scores, respectively; the paw swelling were 35.32±7.05, 72.46±14.47 and 51.65±10.31, respectively; the relative expression levels of miR-885-5p were 1.00±0.18, 0.52±0.10 and 0.71±0.14, respectively. The relative expression levels of suppressor of cytokine signaling 1 (SOCS1) protein in the control, model group, experimental-H group, inh-NC group and inh-miR-885-5p group were 1.00±0.18, 0.51±0.10, 0.75±0.15, 0.71±0.14 and 0.55±0.11, respectively; the levels of interleukin (IL)-6 were (35.29±7.05), (215.82±43.15), (121.33±24.25), (115.62±23.08) and (207.39±41.36) pg·mL-1, respectively; the apoptosis rates were (31.47±6.29)%, (12.19±2.43)%, (22.03±4.41)%, (20.16±4.03)% and (13.37±2.66)%, respectively. The above indexes in the experimental-L, -M, -H groups were dose-dependent, and the differences in the above indexes between the experimental-H group and the control group were statistically significant compared with the model group (P<0.05, P<0.01, P<0.001), and the differences in the above indexes between the inh-miR-885-5p group and the inh-NC group were also all statistically significant (all P<0.05).
Conclusion Sin can regulate macrophage polarization, and improve synovial inflammation in CIA rats, which may be related to the up-regulation of miR-885-5p expression and activation of SOCS1/signal transducer and activator of transcription 3 (STAT3) signaling pathway.
, authors=Jin-feng WANG, Jie LIU, Feng WANG, Xiao-qing LIU, Teng-mao MA, authorsList=Jin-feng WANG, Jie LIU, Feng WANG, Xiao-qing LIU, Teng-mao MA, authorCompany=null, correspAuthors=Jin-feng WANG, 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=1291404586435203444, articleId=1291404583159452015, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=青藤碱调控巨噬细胞极化对胶原诱导性关节炎大鼠的影响, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 探究青藤碱（Sin）通过调控巨噬细胞极化治疗胶原诱导性关节炎（CIA）大鼠的可能作用机制。
方法 将Wistar大鼠随机分为对照组（正常饲养）、模型组（尾根部注射牛Ⅱ型胶原建立CIA模型）和低、中、高剂量实验组（在模型组基础上，分别灌胃40、80、160 mg·kg-1 Sin）以及inh-NC组和inh-miR-885-5p组[在高剂量实验组基础上，分别尾静脉注射微小RNA-885-5p（miR-885-5p）阴性对照和miR-885-5p抑制药]，持续4周，每组各10只。统计各组大鼠关节炎指数（AI）及足跖肿胀度，用苏木精-伊红染色法观察踝关节滑膜组织病理状况，用实时荧光定量聚合酶链反应检测大鼠滑膜组织中miR-885-5p相对表达水平，用蛋白质印迹法检测大鼠滑膜组织中相关蛋白相对表达水平，用酶联免疫吸附试验法检测血清炎症因子水平，用末端脱氧核苷酸转移酶介导的缺口末端标记法检测大鼠滑膜细胞凋亡情况。
结果 对照组、模型组、高剂量实验组的AI评分分别为0、（7.20±1.38）和（5.50±1.10）分，足跖肿胀度分别为35.32±7.05、72.46±14.47和51.65±10.31，miR-885-5p相对表达水平分别为1.00±0.18、0.52±0.10和0.71±0.14；对照组、模型组、高剂量实验组、inh-NC组和inh-miR-885-5p组的细胞因子信号传导抑制因子1（SOCS1）蛋白相对表达水平分别为1.00±0.18、0.51±0.10、0.75±0.15、0.71±0.14和0.55±0.11，白细胞介素（IL）-6水平分别为（35.29±7.05）、（215.82±43.15）、（121.33±24.25）、（115.62±23.08）和（207.39±41.36）pg·mL-1，细胞凋亡率分别为（31.47±6.29）%、（12.19±2.43）%、（22.03±4.41）%、（20.16±4.03）%和（13.37±2.66）%。低、中、高剂量实验组的上述指标呈剂量依赖性变化，高剂量实验组和对照组的上述指标与模型组相比，在统计学上差异均有统计学意义（P<0.05，P<0.01，P<0.001）；inh-miR-885-5p组的上述指标与inh-NC组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 Sin能够调控巨噬细胞极化，改善CIA大鼠滑膜炎症，其机制可能与上调miR-885-5p表达，激活SOCS1/信号转导及转录激活因子3（STAT3）信号途径有关。
, authors=王金凤, 刘杰, 王枫, 刘晓庆, 马腾茂, authorsList=王金凤, 刘杰, 王枫, 刘晓庆, 马腾茂, authorCompany=null, correspAuthors=王金凤, authorNote=
王金凤（1975-），女，副教授，主要从事中西医结合临床方面的研究
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