Research on the Molecular Mechanism of Ginsenoside Ro in Neuronal Damage Following Subarachnoid Hemorrhage

Previous studies have demonstrated the anti-inflammatory, antidepressant, and neuroprotective effects of Ginsenoside Ro. Subarachnoid hemorrhage (SAH), a stroke subtype characterized by bleeding into the subarachnoid space following rupture of intracranial vessels, results in early brain injury (EBI), which critically influences prognosis. Currently, specific treatments for SAH-induced EBI are lacking. This study aimed to investigate the mechanism by which Ginsenoside Ro ameliorates neural injury following SAH, utilizing network pharmacology, molecular docking, qRT-PCR, and Western blot. In this study, we identified 88 common interaction targets between Ginsenoside Ro and SAH. Protein-protein interaction (PPI) network analysis revealed core targets, including TNF-α, EGFR, Bcl-2, SRC, and MMP9. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses indicated that these targets are involved in biological processes such as apoptosis, inflammatory response, and blood-brain barrier repair, primarily modulating the MAPK, PI3K-Akt, and estrogen signaling pathways. Molecular docking confirmed strong binding affinity between Ginsenoside Ro and the core targets SRC, EGFR, MMP9, and Bcl-2. Results demonstrated that Ro significantly modulates the expression of EGFR and Bcl-2, and Ginsenoside Ro could significantly enhance cell viability. These findings suggest that Ginsenoside Ro may mitigate SAH-induced neural injury by regulating the EGFR and Bcl-2 pathways, providing a theoretical foundation for potential clinical applications.