FGF2 Functions in H2S's Attenuating Effect on Brain Injury Induced by Deep Hypothermic Circulatory Arrest in Rats.

Abstract

Deep hypothermic circulatory arrest (DHCA) can protect the brain during cardiac and aortic surgery by cooling the body, but meanwhile, temporary or permanent brain injury may arise. H₂S protects neurons and the central nervous system, especially from secondary neuronal injury. We aim to unveil part of the mechanism of H₂S's attenuating effect on brain injury induced by DHCA by exploring crucial target genes, and further promote the clinical application of H₂S in DHCA. Nine SD rats were utilized to provide histological and microarray samples, and further the differential expression analysis. Then we conducted GO and KEGG pathway enrichment analyses on candidate genes. The protein-protein interaction (PPI) networks were performed by STRING and GeneMANIA. Crucial target genes' expression was validated by qRT-PCR and western blot. Histological study proved DHCA's damaging effect and H₂S's repairing effect on brain. Next, we got 477 candidate genes by analyzing differentially expressed genes. The candidate genes were enriched in 303 GO terms and 28 KEGG pathways. Then nine genes were selected as crucial target genes. The function prediction by GeneMANIA suggested their close relation to immunity. FGF2 was identified as the crucial gene. FGF2 plays a vital role in the pathway when H₂S attenuates brain injury after DHCA. Our research provides more information for understanding the mechanism of H₂S attenuating brain injury after DHCA. We infer the process might probably be closely associated with immunity.