Administration of emodin reduced myocardial infarct size in a dose-dependent manner in mice with AMI, significantly inhibited tumor necrosis factor (TNF)-α expression and NF-κB activation in localized myocardial infarct areas, and inhibited cardiomyocyte apoptosis by inhibiting caspase-3 activation (Wu et al., 2007). Here, TNF is linked to myocardial infarction.