Article(id=1291706983736959917, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706966187991876, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.24.009, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1754582400000, receivedDateStr=2025-08-08, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896543678, onlineDateStr=2026-08-05, pubDate=1766851200000, pubDateStr=2025-12-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896543678, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896543678, creator=13701087609, updateTime=1785896543678, 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=3506, endPage=3511, ext={EN=ArticleExt(id=1291706984420631471, articleId=1291706983736959917, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of the effects of esculetin regulating the JAK2/STAT3 signaling pathway on myocardial ischemia-reperfusion injury in rats, 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 esculetin on myocardial ischemia-reperfusion injury in rats by regulating the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway.
Methods A total of 60 rats were randomly divided into control group, model group, low-dose (L)-esculetin (20 mg·kg-1) experimental group, high-dose (H)-esculetin (40 mg·kg-1) experimental group, and H-esculetin+inhibitor (40 mg·kg-1 esculetin and 20 mg·kg-1 JAK2/STAT3 inhibitor WP1066) group, with 12 rats in each group. Except for the control group, rats in all other groups were subjected to myocardial ischemia-reperfusion modeling. Triphenyltetrazolium chloride (TTC) staining was used to evaluate infarct size; hematoxylin-eosin staining (HE) staining was used to observe histopathological changes; TdT-mediated dUTP Nick-End Labeling (TUNEL) staining was used to observe myocardial apoptosis; enzyme linked immunosorbent assay (ELISA) was used to detect inflammatory cytokines; Western blot was used to detect protein expression of JAK2/STAT3 pathway in rat myocardium.
Results The cardiomyocytes of the rats in the model group were enlarged and arranged in a disorderly manner, while the myocardial damage of rats in the L-esculetin group and the H-esculetin experimental group was reduced. The myocardial infarction areas of the rats in the control group, model group, L-esculetin experimental group, H-esculetin experimental group and H-esculetin+inhibitor group were (3.24±0.35)%, (31.36±3.51)%, (20.75±2.37)%, (10.48±1.16)% and (29.56±3.27)%, respectively; the cardiomyocyte apoptosis rates were (6.37±0.75)%, (56.24±6.03)%, (38.72±3.94)%, (21.46±2.37)% and (51.05±5.28)%, respectively, the levels of interleukin-1β (IL-1β) were (9.34±1.02), (158.95±16.83), (125.49±13.26), (94.83±10.54) and (151.27±16.42) pg·mL-1, respectively; the levels of interleukin-18 (IL-18) were (13.27±1.46), (568.93±59.95), (486.38±51.32), (312.63±33.41) and (527.46±56.25) pg·mL-1, respectively; the levels of tumor necrosis factor-α (TNF-α) were (7.85±0.98), (124.84±14.64), (88.95±9.63), (53.58±5.97) and (116.32±13.27) pg·mL-1, respectively; the relative expression levels of pentraxin 3 (PTX3) protein were 0.86±0.11, 0.32±0.04, 0.53±0.07, 0.71±0.08 and 0.69±0.08, respectively; the relative expression levels of phospho-JAK2 (p-JAK2) protein were 0.81±0.09, 0.36±0.05, 0.54±0.07, 0.73±0.08 and 0.39±0.05, respectively; the relative expression levels of phospho-STAT3 (p-STAT3) protein were 0.78±0.09, 0.29±0.04, 0.52±0.06, 0.74± 0.09 and 0.33±0.04, respectively. Comparing the control group with the model group, the model group with the L-phenithin experimental group, the L-phenithin group with the H-phenithin experimenal group, and the H-phenithin experimental group with the H-phenithin+inhibitor group, there were statistically significant differences in the above indicators (all P<0.05).
Conclusion Esculetin alleviates myocardial ischemia-reperfusion injury in rats by activating the JAK2/STAT3 signaling pathway.
, authors=Peng TIAN
1, Ning-ning WANG
1, Fei-fei MIAO
1, Qing-lu LI
1, Da ZHENG
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目的 探究秦皮乙素调节Janus激酶2（JAK2）/信号转导及转录激活因子3（STAT3）信号通路对大鼠心肌缺血再灌注损伤的影响。
方法 将60只大鼠随机分为对照组、模型组、低剂量（L）-秦皮乙素（20 mg·kg-1）实验组、高剂量（H）-秦皮乙素（40 mg·kg-1）实验组和H-秦皮乙素+抑制剂（40 mg·kg-1秦皮乙素和20 mg·kg-1 JAK2/STAT3抑制剂WP1066）组，每组12只，除对照组外，其余组大鼠均进行心肌缺血再灌注造模。用红四氮唑（TTC）染色法评估梗死面积；用苏木精伊红（HE）染色法观察组织病理变化；用末端脱氧核苷酸转移酶介导的dUTP原位切口末端标记（TUNEL）染色法观察心肌细胞凋亡；用酶联免疫实验法（ELISA）测定炎性细胞因子；用蛋白质印迹法检测大鼠心肌中JAK2/STAT3通路的蛋白表达。
结果 模型组大鼠心肌细胞增大且排列杂乱，L-秦皮乙素实验组、H-秦皮乙素实验组大鼠心肌损伤减轻。对照组、模型组、L-秦皮乙素实验组、H-秦皮乙素实验组和H-秦皮乙素+抑制剂组大鼠心肌梗死面积分别为（3.24±0.35）%、（31.36±3.51）%、（20.75±2.37）%、（10.48±1.16）%和（29.56±3.27）%；心肌细胞凋亡率分别为（6.37±0.75）%、（56.24±6.03）%、（38.72±3.94）%、（21.46±2.37）%和（51.05±5.28）%；白细胞介素-1β（IL-1β）的水平分别为（9.34±1.02）、（158.95±16.83）、（125.49±13.26）、（94.83±10.54）和（151.27±16.42）pg·mL-1；白细胞介素-18（IL-18）的水平分别为（13.27±1.46）、（568.93±59.95）、（486.38±51.32）、（312.63±33.41）和（527.46±56.25）pg·mL-1；肿瘤坏死因子-α（TNF-α）的水平分别为（7.85±0.98）、（124.84±14.64）、（88.95±9.63）、（53.58±5.97）和（116.32±13.27）pg·mL-1；五聚蛋白3（PTX3）蛋白相对表达水平分别为0.86±0.11、0.32±0.04、0.53±0.07、0.71±0.08和0.69±0.08；磷酸化JAK2（p-JAK2）蛋白相对表达水平分别为0.81±0.09、0.36±0.05、0.54±0.07、0.73±0.08和0.39±0.05；磷酸化STAT3（p-STAT3）蛋白相对表达水平分别为0.78±0.09、0.29±0.04、0.52±0.06、0.74±0.09和0.33±0.04；对照组与模型组比较、模型组与L-秦皮乙素实验组比较、L-秦皮乙素实验组与H-秦皮乙素实验组比较、H-秦皮乙素实验组与H-秦皮乙素+抑制剂组比较，上述指标在统计学上差异均有统计学意义（均P<0.05）。
结论 秦皮乙素通过激活JAK2/STAT3信号通路减轻心肌缺血再灌注大鼠损伤。
, authors=田鹏
1, 王宁宁
1, 苗菲菲
1, 李庆禄
1, 郑达
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田鹏（1990-），男，副主任检验师，主要从事免疫学和分子生物学内容的研究
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