Targeting MAPK14 in microglial cells: neuroimmune implications of Panax ginseng in post-stroke inflammation.

This study investigates the molecular mechanisms by which Panax ginseng and its component Panax notoginseng saponin (PNS), particularly Ginsenoside Rc, mitigate neuroinflammatory damage and promote neural repair following ischemic stroke (cerebral infarction). Using bioinformatics analyses—including single-cell RNA sequencing, transcriptomics, and weighted gene co-expression network analysis (WGCNA)—the research identifies MAPK14 as a critical mediator of neuroinflammation in ischemic stroke. Molecular docking and dynamics simulations reveal that Ginsenoside Rc and related ginsenosides bind stably to MAPK14, and in vitro experiments with BV2 microglial cells demonstrate that Ginsenoside Rc treatment, especially combined with MAPK14 silencing, reduces inflammatory cytokine production, reactive oxygen species, and cell death induced by lipopolysaccharide. These findings suggest that targeting MAPK14 with Ginsenoside Rc offers a promising therapeutic strategy to attenuate neuroinflammation and improve cognitive recovery after ischemic stroke, supporting the potential clinical application of Panax ginseng-derived compounds in stroke care.