MAP1LC3B and myocardial infarction: Because both necroptosis and autophagy are mechanisms of delayed ischemic brain injury, we observed the alterations of LC3β expression levels and serum CK levels, respectively, at 12, 24, 48, and 72 h reperfusion after MI, and found that the administration of Nec-1 at the onset of reperfusion significantly reduced the release of creatine kinase and downregulation of autophagy at 12 and 24 h after reperfusion, but the effects were not sustained to 48 and 72 h after reperfusion.