Article(id=1291706975730029323, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706966187991876, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.24.008, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1754496000000, receivedDateStr=2025-08-07, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896541769, onlineDateStr=2026-08-05, pubDate=1766851200000, pubDateStr=2025-12-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896541769, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896541769, creator=13701087609, updateTime=1785896541769, updator=13701087609, issue=Issue{id=1291706966187991876, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='24', pageStart='3451', pageEnd='3600', issueExtLink='null', onlineDate='null', pubDate='1766851200000', pubDateStr='2025-12-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896539494, creator='13701087609', updateTime=1785998798662, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292135872292479273, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706966187991876, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292135872296673578, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706966187991876, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=3499, endPage=3505, ext={EN=ArticleExt(id=1291706975931355916, articleId=1291706975730029323, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of effects of acacetin on lung injury in mice with
Mycoplasma pneumoniae pneumonia by regulating the JAK2/STAT3 signaling pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To discuss the effects of acacetin on lung injury in Mycoplasma pneumoniae pneumonia (MPP) mice and analyze the relationship between its mechanism and the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway.
Methods A MPP mouse model was constructed, and successfully modeled mice were stochastically divided into model group, low, medium and high dose acacetin experimental groups (acacetin-L, M, and H groups: 12.5, 25.0, and 50.0 mg·kg-1 acacetin) and high-dose acacetin-H+JAK2 activator coumarin group (acacetin-H+coumarin 50 mg·kg-1 acacetin-L and 2 mg·kg-1 coumarin), each with 12 mice. Twelve normal healthy mice were intranasally instilled with an equal amount of physiological saline as the control group. Blood gas analyzer was used to detect arterial partial pressure of carbon dioxide (PaCO2) and arterial partial pressure of oxygen (PaO2) of mice, oxygen concentration analyzer was used to detect fraction of inspired oxygen (FiO2), and the oxygenation index (OI) was calculated. Enzyme-linked immunosorbent assay (ELISA) was used to detect serum inflammatory factors. Biochemical method was used to detect oxidative stress indicators. The lung index and lung wet dry ratio were weighed and calculated. Hematoxylin-eosin (HE) staining was employed to evaluate the pathological lesions in lung tissue. Western blot assay was performed to detect the protein expression of JAK2/STAT3 signaling pathway-related molecules.
Results The OI value of the acacetin-L, -M, -H groups, control group, model group, and acacetin-H+coumamycin group were (274.63±30.02), (320.16±35.79), (374.55±39.88), (403.57±43.61), (220.31±26.78) and (241.03±29.14)mmHg, respectively; the IL-6 levels were (124.56±13.27), (87.61±9.23), (56.34±6.77), (36.50±4.15), (172.59±18.24) and (149.33±16.05)pg·mL-1, respectively; the MDA contents were (4.06±0.45), (2.97±0.31), (1.93±0.22), (1.82±0.20), (5.31±0.58) and (4.69±0.49) nmol·mL-1, respectively; the lung index was 1.31±0.15, 0.99±0.11, 0.57±0.07, 0.52±0.06, 1.78±0.19, and 1.54±0.17, respectively; the lung wet/dry weight ratio was (6.83±0.73)%, (5.61±0.58)%, (4.35±0.49)%, (4.10±0.45)%, (7.86±0.86)% and (7.33±0.81)%, respectively; the phosphorylated(p)-JAK2/JAK2 ratio were 0.71±0.08, 0.56±0.06, 0.43±0.05, 0.39±0.04, 0.86±0.09 and 0.79±0.08, respectively; the p-STAT3/STAT3 ratio were 0.67±0.07, 0.46±0.06, 0.30±0.04, 0.16±0.02, 0.83±0.09 and 0.74±0.08, respectively. There were statistically significant differences in the above indicators between the model group and the control group, between the acacetin-H group and the model group, and between the acacetin-H+coumarin group and the acacetin-H group (all P<0.05).
Conclusion Acacetin can effectively improve lung injury in MPP mice, possibly by inhibiting the JAK2/STAT3 signaling pathway.
, authors=Ying-qiao YANG
1, Yan LI
2, Yi-ming HU
3, authorsList=Ying-qiao YANG, Yan LI, Yi-ming HU, authorCompany=null, correspAuthors=Ying-qiao YANG, 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=1291706976258511629, articleId=1291706975730029323, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=刺槐素调节JAK2/STAT3信号通路对肺炎支原体肺炎小鼠肺损伤影响的研究, 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 探究刺槐素对肺炎支原体肺炎（MPP）小鼠肺损伤的影响，分析其机制与Janus激酶2（JAK2）/信号转导子和转录激活子3（STAT3）信号通路的关系。
方法 构建MPP小鼠模型，将造模成功小鼠随机分为模型组、刺槐素低、中、高剂量实验组（12.5、25.0、50.0 mg·kg-1刺槐素）、刺槐素高剂量+JAK2激活剂香豆霉素组（50 mg·kg-1刺槐素和2 mg·kg-1香豆霉素），每组12只，再取12只正常健康小鼠鼻腔滴入等量生理盐水作为对照组；对各组小鼠用血气分析仪检测动脉血二氧化碳分压（PaCO2）、动脉血氧分压（PaO2），氧气浓度分析仪检测吸入氧浓度（FiO2），计算氧合指数（OI）；酶联免疫吸附试验（ELISA）检测血清炎症因子水平；生物化学法检测氧化应激指标；称重计算肺指数和肺湿干比；苏木精伊红（HE）染色观察肺组织病理损伤情况；蛋白质免疫印迹法检测JAK2/STAT3信号通路相关蛋白表达。
结果 刺槐素低、中、高剂量实验组、对照组、模型组和刺槐素高剂量+香豆霉素组的OI值分别为（274.63±30.02）、（320.16±35.79）、（374.55±39.88）、（403.57±43.61）、（220.31±26.78）和（241.03±29.14）mmHg；IL-6水平分别为（124.56±13.27）、（87.61±9.23）、（56.34±6.77）、（36.50±4.15）、（172.59±18.24）和（149.33±16.05）pg·mL-1；MDA含量分别为（4.06±0.45）、（2.97±0.31）、（1.93±0.22）、（1.82±0.20）、（5.31±0.58）和（4.69±0.49）nmol·mL-1；肺指数分别为1.31±0.15、0.99±0.11、0.57±0.07、0.52±0.06、1.78±0.19和1.54±0.17；肺湿干比分别为（6.83±0.73）%、（5.61±0.58）%、（4.35±0.49）%、（4.10±0.45）%、（7.86±0.86）%和（7.33±0.81）%；磷酸化（p）-JAK2/JAK2比值分别为0.71±0.08、0.56±0.06、0.43±0.05、0.39±0.04、0.86±0.09和0.79±0.08；p-STAT3/STAT3比值分别为0.67±0.07、0.46±0.06、0.30±0.04、0.16±0.02、0.83±0.09和0.74±0.08；模型组的上述指标与对照组比较，刺槐素高剂量实验组的上述指标与模型组比较，刺槐素高剂量+香豆霉素组的上述指标与刺槐素高剂量实验组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 刺槐素能够有效改善MPP小鼠肺损伤，可能是通过抑制JAK2/STAT3信号通路来实现的。
, authors=杨颖乔
1, 李燕
2, 胡一明
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杨颖乔（1971-），男，副主任医师，从事呼吸内科相关的临床工作和研究
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