JAK and ERK1/2:how intervention on these two pathways affects myocardial p-STAT3 and TNF-α expression in ischemia-reperfusion

Objective To investigate how the interaction between Janus kinase / signal transducer and activator of transcription (JAK/STAT) pathway and extracellular signal-regulated kinase 1/2 (ERK1/2) signal transduction path-way affects myocardial p-STAT3 and TNF-α protein contents in ischemia-reperfusion. Methods The Langendorff isolated myocardial ischemia-perfusion model was applied. Forty SD rats were randomly divided into normal control group,ischemia-reperfusion group,JAK inhibitor group,ERK1/2 inhibitor group,and JAK-ERK1/2 interaction group. Myocardial p-STAT3 protein content was determined with Western blotting and myocardial TNF-α protein content with ELISA. Results Compared with normal control group,the myocardial p-STAT3 level and TNF-α protein content in the ischemia-reperfusion group was significantly higher (P0.01). The elevated p-STAT3 level and TNF-α protein content were evidently lowered in JAK inhibitor group and the interaction group compared with the ischemia-reperfu-sion group (P0.01,P0.05) and also showed statistical difference when comparison was made between the two groups (P0.05),whereas the p-STAT3 and TNF-α protein in ERK1/2 inhibitor group appeared comparable to the ischemia-reperfusion group (P0.05). Conclusion Myocardial ischemia-reperfusion injury may result in obvious elevation in p-STAT3 and TNF-α protein contents. Inhibition of JAK / STAT signal transduction pathway may significantly reduce p-STAT3 and TNF-α protein content,and at the same time inhibit ERK1/2 signaling pathway in favor of myocardial pro-tection.