Research on the potential mechanisms of propofol in treating depression after brain injury based on network pharmacology

This is the authors' abstract. We don't add key points for this paper.

BACKGROUND: The precise mechanisms by which propofol exerts neuroprotective and antidepressant effects have not been fully elucidated. This study aimed to clarify how propofol alleviates depression following brain injury using a network pharmacology approach. METHODS: By implementing strategies rooted in network pharmacology, we predicted shared target genes of propofol relevant to the treatment of traumatic brain injury, ischemic brain injury, and depression. We analyzed interactions and pathway enrichment through protein-protein interaction networks, along with Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. Potential protein targets were subjected to molecular docking with propofol using AutoDock Vina software. RESULTS: After screening, we identified 22 intersection targets corresponding to 88 Gene Ontology entries and 20 Kyoto Encyclopedia of Genes and Genomes signaling pathways. The key targets primarily include core proteins such as gamma-aminobutyric acid receptors, glutamate receptors, dopamine receptors, and cation channels. Molecular docking simulations confirmed the stable binding of propofol to the 10 key targets. CONCLUSION: This study sheds light on the possible mechanisms by which propofol affects depression in the aftermath of brain injury. Future studies should utilize a network pharmacology framework to explore further the corresponding targets and pathways implicated in the therapeutic effect of propofol on depression after brain injury.