MAPK8 and myocardial infarction: Previous studies have demonstrated that MAPK can be activated by stress and inflammatory stimuli [29] while several studies have documented that myocardial I/R is associated with MAPK activation [46,47], and pharmacological inhibition of JNK is beneficial for limiting I/R injury [48,49] We report that along with reduced myocardial infarct size, acute lycopene administration also significantly inhibited JNK phosphorylation at Thr183/Tyr185 during reperfusion, which is consistent with previous findings that lycopene treatment inhibits H2O2 induced JNK phosphorylation [50].