Article(id=1292130392836956317, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130254689165893, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.05.013, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1768924800000, receivedDateStr=2026-01-21, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785997492274, onlineDateStr=2026-08-06, pubDate=1773676800000, pubDateStr=2026-03-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785997492274, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785997492274, creator=13701087609, updateTime=1785997492274, updator=13701087609, issue=Issue{id=1292130254689165893, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='5', pageStart='601', pageEnd='750', issueExtLink='null', onlineDate='null', pubDate='1773676800000', pubDateStr='2026-03-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785997459337, creator='13701087609', updateTime=1786014469153, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201599108141219, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130254689165893, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201599108141220, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130254689165893, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=671, endPage=677, ext={EN=ArticleExt(id=1292130393029894302, articleId=1292130392836956317, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of effects and mechanism of shionone on rats with ulcerative colitis based on the ERK/NLRP3/IL-1β signaling pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the effects and mechanism of shionone on ulcerative colitis in rats based on the extracellular regulated protein kinase (ERK)/NOD-like receptor protein 3 (NLRP3)/interleukin (IL)-1β signaling pathway.
Methods A total of 60 rats were randomly divided into normal group, model group, experimental-L group, experimental-H group and activator group by random number table method, with 12 rats in each group. The normal group was given drinking water without dextran sulfate sodium, while the other groups were fed with drinking water containing 5% dextran sulfate sodium for 10 days to establish ulcerative colitis rat models. After modeling, rats were administered for 7 days. The experimental-L and -H groups were intragastrically given 50 and 100 mg·kg-1 shionone daily, respectively; the activator group was intragastrically given 100 mg·kg-1 shionone daily combined with intraperitoneal injection of 4 mg·kg-1 ERK activator RO 67-7476; the normal group and model group were intragastrically given and intraperitoneally injected with equal volumes of normal saline daily. Disease activity index was analyzed; the levels of IL-17 and IL-23 in colon tissue were detected by enzyme-linked immunosorbent assay (ELISA); colonic histopathological changes were observed by hematoxylin-eosin (HE) staining; intestinal mucosa was detected by Alcian blue-periodic acid-Schiff (AB-PAS) staining; the relative expression levels of phosphorylated (p)-ERK, NLRP3 and IL-1β proteins were determined by Western blot.
Results Rats in the model group showed severe colonic tissue damage, characterized by disappearance of intestinal mucosa, blurred epithelial cell structure, gland atrophy, inflammatory cell infiltration, lamellar necrosis of the colonic mucosal layer and decreased number of goblet cells. The disease activity index scores in the normal group, model group, experimental-L group, experimental-H group and activator group were (0.12±0.02), (2.98±0.34), (1.76±0.19), (0.55±0.07) and (2.69±0.29) points, respectively; the levels of IL-17 in colon tissue were (24.64±2.74), (39.78±4.27), (32.92±3.65), (26.13±2.85) and (37.85±3.98) pg·mL-1, respectively; the levels of IL-23 in colon tissue were (14.25±1.73), (28.47±3.04), (22.14±2.42), (15.96±1.87) and (26.95±2.94) pg·mL-1, respectively; the histopathological scores of colon tissue were (0±0), (3.73±0.39), (2.49±0.28), (1.24±0.15) and (3.61±0.38) points, respectively; the p-ERK/ERK in colon tissue were 0.32±0.04, 0.81±0.09, 0.58±0.07, 0.36±0.05 and 0.77±0.08, respectively; the relative expression levels of NLRP3 protein were 1.03±0.11, 2.05±0.23, 1.64±0.18, 1.24±0.14 and 1.95±0.22, respectively; the relative expression levels of IL-1β protein were 1.05±0.11, 1.96±0.22, 1.58±0.17, 1.21±0.13 and 1.91±0.21, respectively. Statistical significance was observed in the above indicators when comparing the normal group with the model group, comparing the model group with the experimental-L, H groups and comparing the experimental-H group with the activator group (all P<0.05).
Conclusion Shionone has protective effects on rats with ulcerative colitis by inhibiting the ERK/NLRP3/IL-1β signaling pathway.
, authors=Xiao-hong SUN
1, Xiao-hua ZHANG
2, Qing-na SU
2, Li Shi
3, authorsList=Xiao-hong SUN, Xiao-hua ZHANG, Qing-na SU, Li Shi, authorCompany=null, correspAuthors=Li Shi, 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=1292130393264775327, articleId=1292130392836956317, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=紫菀酮基于ERK/NLRP3/IL-1β信号通路对溃疡性结肠炎大鼠的作用及其机制研究, 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 基于细胞外信号调节激酶(ERK)/NOD样受体热蛋白结构域相关蛋白3(NLRP3)/白细胞介素(IL)-1β信号通路探究紫菀酮对溃疡性结肠炎大鼠的作用及其机制。
方法 将60只大鼠按随机数表法分为正常组、模型组、低、高剂量实验组和激活剂组,每组12只。正常组给予无葡聚糖硫酸钠饮用水,其余各组采用喂食10 d溶解有5%葡聚糖硫酸钠饮用水构建溃疡性结肠炎大鼠模型。造模后给药7 d,低、高剂量实验组分别每日灌胃50、100 mg·kg-1紫菀酮;激活剂组每日灌胃100 mg·kg-1紫菀酮同时腹腔注射4 mg·kg-1 ERK激活剂RO 67-7476;正常组与模型组每日灌胃并腹腔注射等体积生理盐水。分析大鼠疾病活动指数;用酶联免疫吸附测定(ELISA)法检测结肠组织IL-17和IL-23的水平;用苏木素-伊红(HE)染色法检测结肠组织病理变化;用阿尔辛蓝-过碘酸雪夫(AB-PAS)染色法检测肠道黏膜组织病理变化;用蛋白质印迹法检测磷酸化(p-)ERK、NLRP3和IL-1β蛋白相对表达水平。
结果 模型组大鼠结肠组织损伤严重,肠黏膜消失,上皮细胞结构模糊,腺体萎缩,炎症细胞浸润,且结肠黏膜层层状坏死,杯状细胞数量减少。正常组、模型组、低、高剂量实验组和激活剂组的大鼠疾病活动指数评分分别为(0.12±0.02)、(2.98±0.34)、(1.76±0.19)、(0.55±0.07)和(2.69±0.29)分;结肠组织IL-17水平分别为(24.64±2.74)、(39.78±4.27)、(32.92±3.65)、(26.13±2.85)和(37.85±3.98)pg·mL-1;结肠组织IL-23水平分别为(14.25±1.73)、(28.47±3.04)、(22.14±2.42)、(15.96±1.87)和(26.95±2.94)pg·mL-1;结肠组织病理学评分分别为(0±0)、(3.73±0.39)、(2.49±0.28)、(1.24±0.15)和(3.61±0.38)分;结肠组织中p-ERK/ERK分别为0.32±0.04、0.81±0.09、0.58±0.07、0.36±0.05和0.77±0.08;NLRP3蛋白相对表达水平分别为1.03±0.11、2.05±0.23、1.64±0.18、1.24±0.14和1.95±0.22;IL-1β蛋白相对表达水平分别为1.05±0.11、1.96±0.22、1.58±0.17、1.21±0.13和1.91±0.21,正常组的上述指标与模型组比较,模型组与低、高剂量实验组比较,高剂量实验组与激活剂组比较,在统计学上差异均有统计学意义(均P<0.05)。
结论 紫菀酮通过抑制ERK/NLRP3/IL-1β信号通路对溃疡性结肠炎大鼠具有保护作用。
, authors=孙晓虹
1, 张晓华
2, 苏清娜
2, 史历
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孙晓虹(1986-),女,主管药师,主要从事药物治疗和分子生物学方面的工作和研究
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