ArticleFrontiers in neurology
Rehmannioside A alleviates neuroinflammation and cognitive impairments after traumatic brain injury by suppressing microglial activation via the MAPK/NF-κB pathway.
Article in Frontiers in neurology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Traumatic brain injury (TBI) triggers a robust neuroinflammatory response characterized by microglial activation, which propagates secondary neuronal damage and contributes to long-term neurological deficits. Rehmannioside A (REA), a principal bioactive compound from Methods: We employed a controlled cortical impact (CCI) model in mice to mimic clinical TBI. Animals were randomized into Sham/Veh, Sham/REA, TBI/Veh, and TBI/REA (40 mg/kg) groups. Neurological and cognitive functions were assessed using the modified Neurological Severity Score (mNSS) and Morris Water Maze (MWM). Cerebral edema was measured, and histopathological changes were evaluated by H&E and Nissl staining. LPS-stimulated BV2 microglial cells were used for Results: REA treatment significantly improved neurological scores, spatial learning and memory, and reduced cerebral edema and neuronal loss in TBI mice. REA suppressed microglial activation Conclusion: REA ameliorates functional deficits and neuropathology following TBI. The neuroprotective effect may involve suppression of microglia-mediated neuroinflammation via inhibition of the MAPK/NF-κB signaling pathway.
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