中国临床药理学杂志2025，Vol.41Issue(24)：3506-3511,6.DOI:10.13699/j.cnki.1001-6821.2025.24.009
秦皮乙素调节JAK2/STAT3信号通路对大鼠心肌缺血再灌注损伤影响的研究
Research of the effects of esculetin regulating the JAK2/STAT3 signaling pathway on myocardial ischemia-reperfusion injury in rats
摘要
Abstract
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-1 β(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.关键词
秦皮乙素/五聚蛋白3/心肌缺血再灌注损伤/Janus激酶2/信号转导及转录激活因子3Key words
esculetin/pentraxin 3/myocardial ischemia-reperfusion injury/Janus kinase 2/signal transducer and activator of transcription 3分类
医药卫生引用本文复制引用
田鹏,王宁宁,苗菲菲,李庆禄,郑达..秦皮乙素调节JAK2/STAT3信号通路对大鼠心肌缺血再灌注损伤影响的研究[J].中国临床药理学杂志,2025,41(24):3506-3511,6.基金项目
衡水市重点研发计划基金资助项目(2024014032Z) （2024014032Z）
