Fourth, transcriptomic analysis showed that exogenous α-DIPA treatment vigorously inhibited the expression levels of abundant ferroptosis-related genes in microglia, such as Acsl4, Slc7a11, Me1, and Cars. Although it’s well known that ferroptosis is tightly related to neuroinflammation-evoked diseases, such as MS and Alzheimer’s disease, however, it remains elusive about whether endogenous α-DIPA is capable of regulating microglial inflammation in the CNS mainly through ferroptosis pathway. This evidence concerns the gene ME1 and Alzheimer disease.