Update publication information. Hemolytic hyperbilirubinemia-induced brain injury (HHIBI) can cause neonatal death, and survivors often have neurological sequelae, including irreversible motor sensitive and cognitive abnormalities. However, the underlying mechanisms remain elusive. By identifying differentially abundant proteins (DAPs), using proteomics, in the brain tissue of HHIBI rats, we aimed to identify the underlying molecular mechanisms of HHIBI. Tandem mass tag (TMT) labelling and LC-MS/MS were performed, and thereafter bioinformatics methods were used to characterize the molecular and functional signatures of HHIBI. In total, 7104 proteins were identified and 6848 were quantified. We detected 138 upregulated and 242 downregulated DAPs. Further, we found that the upregulated DAPs are involved in complement and coagulation cascade pathways. In addition, downregulated DAPs are mainly involved in DNA replication, mismatch repair, base excision repair, and cell cycle pathways. The Protein-Protein Interactions (PPI) network revealed tha