Adenosine postconditioning protects against myocardial ischemia-reperfusion injury though modulate production of TNF-α and prevents activation of transcription factor NF-kappaB.

Adenosine serves a number of important physiological roles in the body, which is the most widely studied endogenous signal molecules, and the underlying mechanism responsible for such cardioprotection needs more understood, particularly adenosine postconditioning in myocardial ischemia/reperfusion model. In the present study we performed to investigate the inflammatory response of adenosine postconditioning on the cardiac TNF-α expression and NF-κB activation. Eighteen rats were randomly divided into 4 groups: (1) Group A: sham operation group; (2) Group B: ischemia/reperfusion group; (3) Group C: postconditioned groups, four cycles of 30-s reperfusion/30-s occlusion were started immediately after release of the index ischemia (n=6 each); (4) Group D: adenosine was infused 40 μg kg(-1) min(-1) 5 min before the onset of reperfusion without subsequent postconditioning cycles. Hearts were removed at the termination of experiments, which were preserved in frozen tube and stored at -70°C refrigerator for Measurement of malonyldialdehyde (MDA), activities of the NF-κB and TNF-α and IL-10 assay. The results of this study indicate that adenosine postconditioning immediately after myocardial ischemia can reduce the myocardial tissue MDA generation and infarct size, improve cardiac function, which is coincidence with conventional postconditioning. The study also found that modulation of NF-κB activation and accordingly reduces inflammatory factor TNF-α expression may be a molecular mechanism of adenosine down-regulation of inflammatory cytokine production.