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

  • J Cell Mol Med. 2021 Feb;25(3):1371-1382. doi: 10.1111/jcmm.16220.
Shining Xiao  1 ,  Chenggui Wang  1 ,  Quanming Yang  1 ,  Haibin Xu  1 ,  Jinwei Lu  1 ,  Kan Xu  1
Affiliations
  • 1. Department of Orthopedic Surgery, School of Medicine, The Second Affiliated Hospital, Zhejiang University, Hangzhou, China.
PMID: 33369103 DOI: 10.1111/jcmm.16220
Abstract

Inflammation and neuronal Apoptosis aggravate the secondary damage after spinal cord injury (SCI). Rehmannioside A (Rea) is a bioactive herbal extract isolated from Rehmanniae radix with low toxicity and neuroprotection effects. Rea treatment inhibited the release of pro-inflammatory mediators from microglial cells, and promoted M2 polarization in vitro, which in turn protected the co-cultured neurons from Apoptosis via suppression of the NF-κB and MAPK signalling pathways. Furthermore, daily intraperitoneal injections of 80 mg/kg Rea into a rat model of SCI significantly improved the behavioural and histological indices, promoted M2 microglial polarization, alleviated neuronal Apoptosis, and increased motor function recovery. Therefore, Rea is a promising therapeutic option for SCI and should be clinically explored.

Keywords
Rehmannioside A; microglia polarization; neuronal apoptosis; spinal cord injury.
Products