Rea regulates microglial polarization and attenuates neuronal apoptosis via inhibition of the NF-κB and MAPK signalings for spinal cord injury repair

Spinal cord injury (SCI) leads to loss of sensory and motor functions, accompanied by secondary injuries like inflammation and apoptosis. Microglial polarization, especially M1 microglia activation, drives neuroinflammation and neuronal damage. Therefore, treatments should inhibit inflammation and improve the neuronal microenvironment. The inflammatory response is mediated by NF-κB and MAPK pathways, which activate pro-inflammatory factors. Inhibiting these pathways is a viable therapeutic strategy against SCI to reduce neuronal inflammation and apoptosis. Rehmannioside A (Rea), isolated from Rehmanniae radix, is a neuroprotective compound. This study assesses Rea's neuroprotective characteristics in vitro and in vivo, indicating it inhibits NF-κB and MAPK pathways, promotes M2 microglia polarization, and attenuates neuronal apoptosis.

• 1
  Rea treatment inhibited the release of pro-inflammatory mediators from microglial cells in vitro and promoted M2 polarization, protecting co-cultured neurons from apoptosis by suppressing NF-κB and MAPK signaling pathways.
• 2
  In a rat model of SCI, daily intraperitoneal injections of Rea (80 mg/kg) improved behavioral and histological indices, promoted M2 microglial polarization, alleviated neuronal apoptosis, and increased motor function recovery.
• 3
  Rea significantly reduced neuronal apoptosis by inhibiting neuroinflammation and alleviating damage caused by SCI.