Rehmannioside A alleviates neuroinflammation and cognitive impairments after traumatic brain injury by suppressing microglial activation via the MAPK/NF-κB pathway

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Rehmannioside A (REA) reduces neuroinflammation and cognitive deficits after traumatic brain injury (TBI) by inhibiting microglial activation.
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In a mouse model of TBI, REA improved neurological function and spatial memory while decreasing cerebral edema and neuronal degeneration.
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REA therapy resulted in a dose-dependent reduction of pro-inflammatory cytokines in LPS-activated microglial cells.
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The neuroprotective effects of REA are associated with decreased phosphorylation of p65 (NF-κB) and p38 (MAPK) in activated microglia.
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The study supports REA as a potential therapeutic candidate for managing TBI and other neuroinflammatory disorders.

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