Preterm infants account for approximately 11% of all births worldwide each year and can be associated with a higher risk of neuropsychiatric disorders, developmental disorders, and lifelong disabilities. Glutamic acid(GLU), an important excitatory neurotransmitter, plays an important role in the normal function of the central nervous system. Excitatory amino acid transporter 2(EAAT2) is the major glutamate transporter protein responsible for the removal of up to 95% of extracellular glutamate, preventing neuronal excitotoxicity and hyperexcitability. Enhancement of EAAT2 expression and transporter function has received much attention as a potential treatment for adult neurological disorders, but its role in preventing brain injury in preterm infants remains to be explored. In this paper, we review the mechanisms related to EAAT2 in brain injury in preterm infants to provide a new direction for research on the prevention of brain injury in preterm infants.