Article(id=1292126430050144432, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.01.015, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1758470400000, receivedDateStr=2025-09-22, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785996547472, onlineDateStr=2026-08-06, pubDate=1768579200000, pubDateStr=2026-01-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785996547472, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785996547472, creator=13701087609, updateTime=1785996547472, updator=13701087609, issue=Issue{id=1292126377440989952, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='1', pageStart='1', pageEnd='147', issueExtLink='null', onlineDate='null', pubDate='1768579200000', pubDateStr='2026-01-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785996534929, creator='13701087609', updateTime=1786014708731, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292202603945947673, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292202603950141978, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=93, endPage=99, ext={EN=ArticleExt(id=1292126430247276721, articleId=1292126430050144432, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research on the effects and mechanism of naringenin on diabetes-related intestinal inflammation, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To analyze the potential mechanism of naringenin in improving diabetes-related intestinal inflammation.
Methods In cell experiment, STC-1 cells were randomized into blank group, advanced glycation end products (AGEs) group, experimental-L group (AGEs+25 μg·mL-1 naringenin) and experimental-H group (AGEs+50 μg·mL-1 naringenin). In animal experiment, male C57BL/6J mice were randomly divided into control group, model group (to construct diabetes-related intestinal injury model), experimental-L group (modeling +25 mg·kg-1 naringenin), experimental-H group (modeling +75 mg·kg-1 naringenin) and metformin group (modeling +0.5 g·kg-1 metformin). STC-1 cell necroptosis was detected using the Hoechst 33342/propidium iodide (PI) double staining method. Glycolipid metabolism indicators and pro-inflammatory factor levels were measured by enzyme-linked immunosorbent assay (ELISA). The expression of phosphorylated mixed lineage kinase domain-like (p-MLKL) protein and Occludin protein was assessed by Western blotting.
Results In cell experiment, PI-positive rates of blank, AGEs, experimental-L and experimental-H groups were (4.36±0.30)%, (19.37±1.58)%, (15.90±1.03)% and (12.85±1.51), respectively; IL-6 levels were (17.74±2.23), (71.46±6.54), (42.39±5.34) and (33.63±1.82) pg·mL-1, respectively; p-MLKL relative expression levels were 0.39±0.05, 0.83±0.10, 0.74±0.07 and 0.58±0.04, respectively. All indicators showed significant differences between AGEs group and blank group, experimental-L group or experimental-H group and AGEs group (P<0.05, P<0.01). In animal experiment, post-intervention FBG levels of blank control group, model group, experimental-L group, experimental-H group and metformin group were (4.89±0.54), (26.88±1.96), (18.47±1.53), (14.96±1.67) and (13.91±1.16) mmol·L-1, respectively; TG levels were (0.43±0.06), (1.70±0.15), (1.46±0.14), (1.13±0.10) and (0.81±0.09) mmol·L-1, respectively; IL-6 levels were (13.59±1.06), (62.02±5.92), (50.19±4.44), (37.78±3.58) and (48.91±8.46) pg·mL-1, respectively; the relative expression levels of p-MLKL were 0.38±0.05, 1.07±0.13, 0.79±0.08, 0.61±0.05 and 0.80±0.09, respectively; the relative expression levels of Occludin were 0.97±0.07, 0.35±0.04, 0.61±0.05, 0.83±0.07 and 0.43±0.06, respectively. Significant differences were observed between model group and blank control group, experimental-L group or experimental-H group or metformin groups and model group (P<0.05, P<0.01).
Conclusion Naringenin can improve the function of intestinal endocrine cells and protect against diabetes-related intestinal injury, which may be related to the mechanism of necrotic apoptosis mediated by MLKL.
, authors=Hai-xin QI
1, Zhi CHEN
1, Yun-fei DONG
1, Zheng-yu FANG
1, Guo-qiang LIN
1, Gui-qun ZHOU
2, authorsList=Hai-xin QI, Zhi CHEN, Yun-fei DONG, Zheng-yu FANG, Guo-qiang LIN, Gui-qun ZHOU, authorCompany=null, correspAuthors=Hai-xin QI, 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=1292126430469574834, articleId=1292126430050144432, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=柚皮素对糖尿病相关肠道炎症的作用及机制研究, 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 分析柚皮素改善糖尿病相关肠道炎症的潜在作用机制。
方法 在细胞实验中，将STC-1细胞随机分为空白组、晚期糖基化终末产物（AGEs）组、低剂量实验组（AGEs+25 μg·mL-1的柚皮素）和高剂量实验组（AGEs+50 μg·mL-1的柚皮素）。在动物实验中，将C57BL/6J雄性小鼠随机分为空白对照组、模型组（构建糖尿病相关肠道损伤模型）、低剂量实验组（建模+25 mg·kg-1的柚皮素）、高剂量实验组（建模+75 mg·kg-1的柚皮素）和二甲双胍组（建模+0.5 g·kg-1的二甲双胍）。用Hoechst 33342/检测碘化丙啶（PI）双染法检测STC-1细胞坏死性凋亡，用酶联免疫吸附法（ELISA）检测糖脂代谢指标和促炎因子水平，用蛋白质印迹法检测磷酸化混合谱系激酶结构域样（p-MLKL）蛋白和闭锁蛋白（Occludin）蛋白表达情况。
结果 在细胞实验中，空白组、AGEs组、低剂量实验组和高剂量实验组的PI阳性率分别为（4.36±0.30）%、（19.37±1.58）%、（15.90±1.03）%和（12.85±1.51）%；IL-6水平分别为（17.74±2.23）、（71.46±6.54）、（42.39±5.34）和（33.63±1.82）pg·mL-1；p-MLKL蛋白相对表达水平分别为0.39±0.05、0.83±0.10、0.74±0.07和0.58±0.04，上述指标在AGEs组与空白组比较，低、高剂量实验组与AGEs组比较，在统计学上差异均有统计学意义（P<0.05，P<0.01）。在动物实验中，干预后，空白对照组、模型组、低剂量实验组、高剂量实验组和二甲双胍组的FBG分别为（4.89±0.54）、（26.88±1.96）、（18.47±1.53）、（14.96±1.67）和（13.91±1.16）mmol·L-1；TG水平分别为（0.43±0.06）、（1.70±0.15）、（1.46±0.14）、（1.13±0.10）和（0.81±0.09）mmol·L-1；IL-6水平分别为（13.59±1.06）、（62.02±5.92）、（50.19±4.44）、（37.78±3.58）和（48.91±8.46）pg·mL-1；p-MLKL蛋白相对表达水平分别为0.38±0.05、1.07±0.13、0.79±0.08、0.61±0.05和0.80±0.09；Occludin蛋白相对表达水平分别为0.97±0.07、0.35±0.04、0.61±0.05、0.83±0.07和0.43±0.06，上述指标在模型组与空白对照组比较，柚皮素低、高剂量实验组及二甲双胍组与模型组比较，在统计学上差异均有统计学意义（P<0.05，P<0.01）。
结论 柚皮素可以改善肠内分泌细胞功能对糖尿病相关肠损伤发挥保护作用，可能与MLKL介导的坏死性凋亡机制有关。
, authors=齐海鑫
1, 陈植
1, 董云飞
1, 方征宇
1, 林国强
1, 周桂群
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齐海鑫（1984-），男，主治中医师，主要从事肛周及肠道炎症性疾病的诊断与治疗方面的工作和研究
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齐海鑫（1984-），男，主治中医师，主要从事肛周及肠道炎症性疾病的诊断与治疗方面的工作和研究
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