Integrative Bioinformatics Analysis Unravel the Association between Intracerebral Hemorrhage and Cellular Apoptosis through Immune Infiltration

Background. Intracerebral hemorrhage (ICH, IH) is a stroke syndrome characterized by high mortality and disability rates. However, the apoptotic mechanisms underlying ICH remain incompletely understood. We employed bioinformatics methods to identify key apoptotic genes associated with ICH, thereby offering potential therapeutic targets and contributing to a deeper understanding of the pathogenic mechanisms of apoptosis in ICH. Materials and Methods. We retrieved microarray data of ICH patients from the Gene Expression Omnibus database and intersected it with apoptotic genes, filtering out apoptosis-related differentially expressed genes (ARDEGs). Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were conducted, and a logic regression-based diagnostic model for ICH was constructed. Key genes were identified through least absolute shrinkage and selection operator regression after model validation. Subsequently, mRNA-transcription factor (mRNA-TF), mRNA–microRNA (mRNA–miRNA), mRNA-RNA-binding protein (mRNA-RBP), and mRNA-drug regulatory networks were established, followed by immune infiltration analysis. Results. We identified 29 ARDEGs related to ICH, primarily participating in biological processes such as the extrinsic apoptotic signaling pathway and neuroinflammatory response. The ICH model confirmed PPP1R15A, IL1R1, and TYROBP as key genes with diagnostic and therapeutic value. Thirteen immune cell types showed a correlation with ICH; notably, activated dendritic cells and CD56dim natural killer cells exhibited significant correlations, and key genes were positively correlated with all 13 immune cell types. The regulatory networks (mRNA-TF, mRNA–miRNA, mRNA-RBP, and mRNA-drug) provided insights into the apoptotic gene regulation mechanisms and potential drugs in ICH. Conclusion. Through bioinformatics analysis, we identified PPP1R15A, IL1R1, and TYROBP as crucial genes in the occurrence and progression of ICH, with the potential involvement of Activated dendritic cells and CD56dim natural killer cells in these processes.