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.

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.

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).

Esculetin alleviates myocardial ischemia-reperfusion injury in rats by activating the JAK2/STAT3 signaling pathway.