Article(id=1292130268647809726, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130221843571059, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.08.014, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1768147200000, receivedDateStr=2026-01-12, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785997462664, onlineDateStr=2026-08-06, pubDate=1777305600000, pubDateStr=2026-04-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785997462664, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785997462664, creator=13701087609, updateTime=1785997462664, updator=13701087609, issue=Issue{id=1292130221843571059, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='8', pageStart='1051', pageEnd='1200', issueExtLink='null', onlineDate='null', pubDate='1777305600000', pubDateStr='2026-04-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785997451505, creator='13701087609', updateTime=1786014411018, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201355276480844, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130221843571059, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201355276480845, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130221843571059, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1137, endPage=1143, ext={EN=ArticleExt(id=1292130269021102784, articleId=1292130268647809726, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of the mechanism of theaflavin improving the inflammatory response of intestinal epithelial cells in ulcerative colitis by regulating the AEG-1-mediated NLRP3/Caspase-1 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 mechanism of theaflavin improving the inflammatory response of intestinal epithelial cells in ulcerative colitis (UC) through regulating NOD-like receptor thermal protein domain associated protein 3 (NLRP3) / Caspase-1 signaling pathway mediated by astrocyte elevated gene 1 (AEG-1).
Methods NCM460 cells were divided into control group (conventional culture of NCM460 cells without any intervention treatment, model group (treated with 1 mg·L-1 lipopolysaccharide in NCM460 cells for 24 hours), experimental group (treated with 64 μmol·L-1 theaflavin and 1 mg·L-1 lipopolysaccharide in NCM460 cells for 24 h), pcDNA3.1-NC group (after NCM460 cells were transfected with the pcDNA3.1-NC plasmid, treated with 64 μmol·L-1 theaflavin and 1 mg·L-1 lipopolysaccharide for 24 h) and pcDNA3.1-AEG-1 group (after NCM460 cells were transfected with the pcDNA3.1-AEG-1 plasmid, treated with 64 μmol·L-1 theaflavin and 1 mg·L-1 lipopolysaccharide for 24 h). Cell viability was detected by cell counting kit-8 method, cell invasion ability was detected by Transwell assay, cell migration ability was detected by cell scratch assay, and mRNA levels of AEG-1 and barrier damage-related proteins were detected by real-time fluorescence quantitative reverse transcription polymerase chain reaction. Western blotting was used to detect the expressions of AEG-1, apoptosis, barrier injury and NLRP3/Caspase-1 signaling pathway-related proteins and enzyme-linked immunosorbent assay was used to detect the contents of inflammatory factors.
Results The cell migration rate of the control group, model group, experimental group were (78.85±13.47)%, (19.32±3.15)% and (54.97±9.03)%, respectively. The levels of interleukin-6 (IL-6) in the control group, model group, experimental group, pcDNA3.1-NC group and pcDNA3.1-AEG-1 group were (0.49±0.07), (1.36±0.21), (0.64±0.09), (0.68±0.10) and (1.21±0.18) pg·L-1, respectively; the apoptosis rates were (8.26±1.47)%, (27.09±4.62)%, (14.51±2.18)%, (16.75±2.83)% and (22.68±3.56)%, respectively; the relative expression levels of B-cell lymphoma-2 (Bcl-2) protein were 1.00±0.16, 0.39±0.07, 0.71±0.12, 0.67±0.09 and 0.54±0.08, respectively; the relative expression levels of Bcl-2-associated X (Bax) protein were 1.00±0.19, 6.45±1.12, 3.90±0.64, 3.79±0.58 and 6.07±0.96, respectively; the mRNA levels of AEG-1 were 1.00±0.13, 4.35±0.76, 1.92±0.33, 2.08±0.32 and 3.26±0.57, respectively; the relative expression levels of AEG-1 protein were 1.00±0.17, 4.82±0.79, 2.07±0.34, 2.25±0.36 and 3.94±0.71, respectively; the mRNA levels of Zonula Occludens-1 (ZO-1) were 1.00±0.15, 0.37±0.06, 0.76±0.13, 0.79±0.14 and 0.51±0.09, respectively, while the mRNA levels of Occludin were 1.00±0.16, 0.29±0.05, 0.58±0.10, 0.52±0.09 and 0.37±0.06, respectively; the relative protein expression levels of NLRP3 were 1.00±0.19, 6.58±1.06, 2.71±0.43, 2.59±0.42 and 5.16±0.94, respectively; the relative protein expression levels of cleaved caspase-1 were 1.00±0.16, 5.26±0.93, 3.42±0.59, 3.65±0.64 and 5.09±0.87, respectively. When comparing the model group with the control group and the experimental group, and the pcDNA3.1-NC group with the pcDNA3.1-AEG-1 group, the differences in the above indicators were all statistically significant (P<0.01, P<0.001).
Conclusion Theaflavin can improve the inflammatory response of LPS-induced UC intestinal epithelial cells and inhibit cell apoptosis, and has a protective effect on epithelial barrier function. The mechanism may be related to the down-regulation of AEG-1 expression and the inhibition of the NLRP3/Caspase-1 signaling pathway.
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目的 探讨茶黄素通过调控星形细胞上调基因1（AEG-1）介导NOD样受体热蛋白结构域相关蛋白3（NLRP3）/半胱天冬蛋白酶-1（Caspase-1）信号通路改善溃疡性结肠炎（UC）肠上皮细胞炎症反应的机制。
方法 将NCM460细胞分为空白组（NCM460细胞常规培养，不进行任何干预处理）、模型组（给予NCM460细胞1 mg·L-1脂多糖处理24 h）、实验组（给予NCM460细胞64 μmol·L-1茶黄素和1 mg·L-1脂多糖处理24 h）、pcDNA3.1-NC组（NCM460细胞转染pcDNA3.1-NC质粒后，给予64 μmol·L-1茶黄素和1 mg·L-1脂多糖处理24 h）、pcDNA3.1-AEG-1组（NCM460细胞转染pcDNA3.1-AEG-1质粒后，给予64 μmol·L-1茶黄素和1 mg·L-1脂多糖处理24 h）。用细胞计数试剂盒8法、Transwell及细胞划痕实验检测细胞活力、侵袭及迁移能力，用实时荧光定量逆转录聚合酶链式反应检测AEG-1、屏障损伤相关蛋白的mRNA水平，用蛋白免疫印迹法检测AEG-1、凋亡、屏障损伤及NLRP3/Caspase-1信号通路相关蛋白表达，用酶联免疫吸附法检测炎症因子含量。
结果 空白组、模型组和实验组的细胞迁移率分别为（78.85±13.47）%、（19.32±3.15）%和（54.97±9.03）%。空白组、模型组、实验组、pcDNA3.1-NC组、pcDNA3.1-AEG-1组的白细胞介素-6（IL-6）水平分别为（0.49±0.07）、（1.36±0.21）、（0.64±0.09）、（0.68±0.10）和（1.21±0.18）pg·L-1，凋亡率分别为（8.26±1.47）%、（27.09±4.62）%、（14.51±2.18）%、（16.75±2.83）%和（22.68±3.56）%，B淋巴细胞瘤-2（Bcl-2）蛋白相对表达水平分别为1.00±0.16、0.39±0.07、0.71±0.12、0.67±0.09和0.54±0.08，Bcl-2相关X（Bax）蛋白的相对表达水平分别为1.00±0.19、6.45±1.12、3.90±0.64、3.79±0.58和6.07±0.96，AEG-1 mRNA分别为1.00±0.13、4.35±0.76、1.92±0.33、2.08±0.32和3.26±0.57，AEG-1蛋白相对表达水平分别为1.00±0.17、4.82±0.79、2.07±0.34、2.25±0.36和3.94±0.71，紧密连接蛋白-1（ZO-1）的mRNA分别为1.00±0.15、0.37±0.06、0.76±0.13、0.79±0.14和0.51±0.09，闭合蛋白（Occludin）的mRNA分别为1.00±0.16、0.29±0.05、0.58±0.10、0.52±0.09和0.37±0.06，NLRP3的蛋白相对表达水平分别为1.00±0.19、6.58±1.06、2.71±0.43、2.59±0.42和5.16±0.94，Cleaved Caspase-1的蛋白相对表达水平分别为1.00±0.16、5.26±0.93、3.42±0.59、3.65±0.64和5.09±0.87。上述指标，模型组与空白组、实验组比较，pcDNA3.1-NC组与pcDNA3.1-AEG-1组比较，在统计学上差异均有统计学意义（P<0.01，P<0.001）。
结论 茶黄素可改善LPS诱导UC肠上皮细胞的炎症反应和抑制细胞凋亡，对上皮屏障功能具有保护作用，其机制可能与下调AEG-1表达抑制NLRP3/Caspase-1信号通路有关。
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童景飞（1983-），男，主治中医师，主要从事溃疡性结肠炎方面的工作和研究
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