High-dose dexamethasone regulates microglial polarization via the GR/JAK1/STAT3 signaling pathway after traumatic brain injury.

ABSTRACT: JOURNAL/nrgr/04.03/01300535-202509000-00023/figure1/v/2024-11-05T132919Z/r/image-tiff Although microglial polarization and neuroinflammation are crucial cellular responses after traumatic brain injury, the fundamental regulatory and functional mechanisms remain insufficiently understood. As potent anti-inflammatory agents, the use of glucocorticoids in traumatic brain injury is still controversial, and their regulatory effects on microglial polarization are not yet known. In the present study, we sought to determine whether exacerbation of traumatic brain injury caused by high-dose dexamethasone is related to its regulatory effects on microglial polarization and its mechanisms of action. In vitro cultured BV2 cells and primary microglia and a controlled cortical impact mouse model were use

SUBMITTER: Yang M 

PROVIDER: S-EPMC11801282 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature