Conclusions
It seems that dysregulation of energy metabolism, especially nitrogen metabolism, may be a major cause in secondary ICH injury. This information provides novel insights into secondary events following ICH.
Methods
To examine one of the gaps in the knowledge about ICH pathological mechanisms, isobaric tag for relative and absolute quantification (iTRAQ)-based liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used in collagenase-induced ICH rats on the 2nd day.
Results
A total of 6,456 proteins were identified with a 1% false discovery rate (FDR). Of these proteins, 126 and 75 differentially expressed proteins (DEPs) were substantially increased and decreased, respectively. Based on Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and STRING analyses, the protein changes in cerebral hemorrhage were comprehensively evaluated, and the energy metabolism in ICH was anchored. The core position of the nitrogen metabolism pathway in brain metabolism in ICH was found for the first time. Carbonic anhydrase 1 (Ca1), carbonic anhydrase 2 (Ca2), and glutamine synthetase (Glul) participated in this pathway. We constructed the protein-protein interaction (PPI) networks for the energy metabolism of ICH, including the Atp6v1a-Atp6v0c-Atp6v0d1-Ppa2-Atp6ap2 network. Conclusions: It seems that dysregulation of energy metabolism, especially nitrogen metabolism, may be a major cause in secondary ICH injury. This information provides novel insights into secondary events following ICH.