The present study drew the following conclusions: (1) neurons ferroptosis can be activated by sepsis in rats; (2) NEAT1, packaged in exosome, passed through BBB and highly expressed in the cerebral cortex of rats with ferroptosis; (3) NEAT1 functions as a ceRNA for miR-9-5p to facilitate TFRC and GOT1 expression; (4) miR-9-5p alleviated sepsis-induced neurons ferroptosis by suppressing the expression of TFRC and GOT1; and (5) the lncRNA NEAT1 might regulates SAE through miR-9-5p/TFRC/GOT1. The gene discussed is NEAT1; the disease is Sepsis.