OBJECTIVE

To explore the role of spinal MAPK-ERK signal pathway in myocardial ischemia-reperfusion (I/R) injury.

METHODS

Sixty male Sprague-Dawley(SD) rats (80-100 g) were randomly divided into 3 groups: sham (n=10), PD98059 (n=25) and I/R groups (n=25). Three days after successful intrathecal implantation, 5 μg DMSO was injected intrathecally into the sham group, and then the left coronary arteries were separated without being tied. Rats in the I/R and PD98059 groups were injected with 5 μL DMSO and PD98059 (5 μg) 30 minutes before thoractomy respectively. Then the left coronary artery was tied for 30 minutes followed by 120 minutes of reperfusion. After the experiments, the ERK phosphorylation condition of T1-T4 spinal cord segments was detected with immunofluorescence; the myocardiac apoptosic index and infarct size were measured.

RESULTS

Expression of p-ERK in the I/R group was significantly higher than in the sham and PD98059 groups (P<0.05). Myocardial apoptotic index and infarct size in the PD98059 group were significantly lower than in the I/R group (P<0.05), but higher in the PD98059 group than in the sham group (P<0.05).

CONCLUSIONS

The MAPK-ERK pathway in the superior thorathic spinal cord can be activated by myocardial ischemia-reperfusion and inhibition of the pathway can play a protective role in myocardial ischemia-reperfusion injury.