Article(id=1292130304253251902, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130221843571059, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.08.011, 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=1785997471153, onlineDateStr=2026-08-06, pubDate=1777305600000, pubDateStr=2026-04-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785997471153, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785997471153, creator=13701087609, updateTime=1785997471153, 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=1114, endPage=1121, ext={EN=ArticleExt(id=1292130307172487487, articleId=1292130304253251902, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of mechanism of morin alleviating airway inflammation in asthma by regulating MDM2 to maintain the integrity of epithelial cell structure, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the potential mechanism of morin in improving airway inflammation in asthma.
Methods In animal experiments, rats were randomly divided into four groups, with 10 rats in each group: animal control group, animal model group [ovalbumins (OVA)-induced], animal experimental-L group (OVA-induced + 10 mg·kg-1 morin), animal experimental-M (OVA-induced+30 mg·kg-1 morin) and the experimental-H group (OVA-induced+100 mg·kg-1 morin). After 4 weeks of treatment, bronchoalveolar lavage fluid (BALF) and serum were collected for subsequent use, and lung tissues were harvested. Western blot assay was used to detect the expression of murine double minute 2(MDM2) protein; enzyme-linked immunosorbent assay (ELISA) assay was employed to determine the expression of inflammatory factors in BALF; and real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) assay was applied to measure the mRNA expressions of tumor protein 53 (p53) and BCL-2 associated X protein (Bax). In cell experiments, 16HBE cells were randomly assigned to four groups: cell blank group, cell model group [treated with 50 μg·L-1 interleukin(IL)-13], cell experimental group (treated with 65 μmol·L-1 morin+IL-13), si-NC group(transfected with si-NC, then treated with 65 μmol·L-1 morin+IL-13) and si-MDM2 group (transfected with si-MDM2, then treated with 65 μmol·L-1 morin+IL-13). After 48 hours of treatment, TdT mediated dUDP nick end labeling(Tunel) assay was used to detect the cell apoptosis rate; Western blot assay was performed to determine protein expression and P53 ubiquitination level.
Results In animal experiments, the levels of MDM2 protein in the animal control group, animal model group, animal experimental-L group, animal experimental-M and animal experimental-H group were 0.65±0.05, 0.32±0.03, 0.41±0.06, 0.46±0.04 and 0.51±0.05, respectively; the levels of BALF-IL-13 were (15.44±1.19), (55.43±3.90), (48.79±4.88), (37.25±4.59) and (25.64±1.64) pg·mL-1, respectively; the relative expression levels of p53 mRNA were 1.00±0.14, 1.75±0.13, 1.51±0.12, 1.44±0.09 and 1.24±0.14, respectively; the relative expression levels of Bax mRNA were 1.00±0.14, 1.94±0.16, 1.75±0.17, 1.62±0.17 and 1.39±0.09, respectively; when comparing the animal model group with the animal control group, and the animal experimental-L, -M, -H groups with the animal model group respectively, the differences of the above indicators were all statistically significant (P<0.05, P<0.01). In cell experiment, the apoptosis rates of cells in cell blank group, cell model group, cell experimental group, si-NC group and si-MDM2 group were (3.94±0.27), (31.76±2.39), (19.93±1.91), (18.14±2.50) and (25.97±1.74)%, respectively; the realtive expression levels of MDM2 protein were 0.91±0.09, 0.44±0.05, 0.66±0.08, 0.68±0.05 and 0.21±0.04, respectively; when comparing the cell model group with the cell blank group, the cell experimental group with the cell model group, the si-MDM2 group with the si-NC group, the differences of the above indicators were all statistically significant (all P<0.01).
Conclusion Morin may alleviate asthmatic airway inflammation and cell apoptosis by upregulating MDM2 ubiquitination to regulate p53.
, authors=Ling ZHAO, Jun-peng CAI, Xiao-min ZHOU, Xiao-jiang LV, authorsList=Ling ZHAO, Jun-peng CAI, Xiao-min ZHOU, Xiao-jiang LV, authorCompany=null, correspAuthors=Xiao-jiang LV, 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=1292130309802316098, articleId=1292130304253251902, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=桑色素通过调节MDM2维持上皮细胞结构完整减轻哮喘气道炎症的机制研究, 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=
方法 在动物实验中，大鼠随机分为动物对照组、动物模型组[卵清蛋白（OVA）诱导]、动物低剂量实验组（OVA诱导+10 mg·kg-1桑色素）、动物中剂量实验组（OVA诱导+30 mg·kg-1桑色素）和高剂量实验组（OVA诱导+100 mg·kg-1桑色素），每组10只，治疗4周后，收集支气管肺泡灌洗液（BALF）、血清备用及取肺组织，用蛋白质印迹法检测鼠双微体基因2（MDM2）蛋白表达，用酶联免疫吸附法测定（ELISA）检测BALF炎性因子表达，用实时荧光定量聚合酶链反应（RT-qPCR）法检测肿瘤蛋白53（p53）、BCL-2相关X蛋白（Bax）mRNA表达。在细胞实验中，将16HBE细胞随机分为细胞空白组、细胞模型组[50 μg·L-1的白细胞介素（IL）-13]、细胞实验组（65 μmol·L-1的桑色素+IL-13）、si-NC组（转染si-NC+65 μmol·L-1的桑色素+IL-13）和si-MDM2组（转染si-MDM2+65 μmol·L-1的桑色素+IL-13），处理48 h后，用原位末端转移酶标记法（Tunel）检测细胞凋亡率，用蛋白质印迹法检测蛋白表达和P53泛素化水平。
结果 在动物实验中，动物对照组、动物模型组、动物低、中、高剂量实验组的MDM2蛋白相对表达水平分别为0.65±0.05、0.32±0.03、0.41±0.06、0.46±0.04和0.51±0.05；BALF-IL-13水平分别为（15.44±1.19）、（55.43±3.90）、（48.79±4.88）、（37.25±4.59）和（25.64±1.64）pg·mL-1；p53 mRNA相对表达水平分别为1.00±0.14、1.75±0.13、1.51±0.12、1.44±0.09和1.24±0.14；Bax mRNA相对表达水平分别为1.00±0.14、1.94±0.16、1.75±0.17、1.62±0.17和1.39±0.09；上述指标，动物模型组与动物对照组比较，动物低、中、高剂量组分别与动物模型组比较，差异均具有统计学意义（P<0.05，P<0.01）。在细胞实验中，细胞空白组、细胞模型组、细胞实验组、si-NC组和si-MDM2组细胞凋亡率分别为（3.94±0.27）、（31.76±2.39）、（19.93±1.91）、（18.14±2.50）和（25.97±1.74）%；MDM2蛋白相对表达水平分别为0.91±0.09、0.44±0.05、0.66±0.08、0.68±0.05和0.21±0.04；上述指标，细胞模型组与空白组比较，细胞实验组与细胞模型组比较，si-MDM2组与si-NC组比较，在统计学上差异均具有统计学意义（均P<0.01）。
结论 桑色素可能通过上调MDM2泛素化调节p53减轻哮喘气道炎症及细胞凋亡。
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赵凌（1988-），男，住院医师，主要从事儿童消化、呼吸疾病方面的工作和研究
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