Effects of edaravone on JAK2/STAT3 signaling pathway in transplanted donor liver of rats with different cold ischemia times / 天津医药

ABSTRACT

Objective To investigate the effect of edaravone on the JAK2/STAT3 signaling pathway after ischemia-reperfusion injury in donor rat liver under different cold ischemia times. Methods A total of 102 SD rats were randomly divided into sham operation group,control group and experimental group. Six rats were in sham operation group with free liver operation and no transplantation. Forty-eight rats were in control group and experimental group respectively, and divided into subgroups according to the different cold ischemia times (30 min, 6 h, 12 h and 18 h). There were 6 donors and 6 recipients in each group. The rat model of orthotopic liver transplantation was established by modifiedtwo cuff method. All the donors were perfused by abdominal aorta and the warm ischemia time was 3-5 min. After different cold ischemia times, the experimental group was treated with edaravone (3 mg/kg) at 5 min before the opening of the new hepatic artery, and control group was injected with 3 mg/kg saline. Recipients of each group were sacrificed after 6 h. Finally, real-time fluorescence quantitative PCR was used to analyze the relative expression of JAK2/STAT3 mRNA of donor liver. Results The GAPDH gene and JAK2/STAT3 were well amplified. Under the same cold ischemia time, compared with the control group, the relative expression of JAK2/STAT3 was significantly decreased in the experimental group (P<0.05). With the prolongation of cold ischemia time, the relative expressions of JAK2 and STAT3 mRNA showed a decreasing trend in control group and experimental group, while the relative expression of JAK2 mRNA increased first and then decreased in the experimental group (P<0.05). Conclusion Edaravone has a protective effect on transplanted donor liver during different cold ischemia times, and extends the cold ischemia time for 18 h, which may be related to the inhibition of JAK2/STAT3 signal transduction pathway.