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Noni Inhibits Neuronal Damage Caused by the Immune Reaction of Microglial Cells Activated by Doxorubicin

Doxorubicin에 의해 활성화된 미세 아교세포의 면역반응으로 인한 신경손상에 Noni가 미치는 영향

  • Jung, Se-Hwa (Department of Biomedical Laboratory Science, Konyang University) ;
  • Lee, Seong-Min (Department of Biomedical Laboratory Science, Konyang University) ;
  • Ha, Ji-Sun (Department of Biomedical Laboratory Science, Konyang University) ;
  • Yang, Seung-Ju (Department of Biomedical Laboratory Science, Konyang University) ;
  • Kim, Pyung-Hwan (Department of Biomedical Laboratory Science, Konyang University)
  • 정세화 (건양대학교 임상병리학과) ;
  • 이성민 (건양대학교 임상병리학과) ;
  • 하지선 (건양대학교 임상병리학과) ;
  • 양승주 (건양대학교 임상병리학과) ;
  • 김평환 (건양대학교 임상병리학과)
  • Received : 2020.09.28
  • Accepted : 2020.10.19
  • Published : 2020.12.31

Abstract

Microglial cells function as major immune cells in the brain, playing an important role in the protection and damage of neurons. BV2 microglia, activated by drug stimulation, secrete inflammatory cytokines by activating the nuclear factor kappa-light-chain-enhancer of the activated B cells pathway and are involved in neuroinflammatory and immune responses. The overactivation of microglia by stimuli can cause neuronal damage, leading to brain disease. Noni, a natural product, reduces the activity of microglia to prevent neuronal damage and is a potential natural medicine because it exerts excellent regeneration and anti-inflammatory effects on damaged cells. In this study, when noni was used to treat BV2 cells stimulated by the anti-cancer drug doxorubicin, it reduced the release of pro-inflammatory cytokines from BV2. On the other hand, neuronal damage is a side effect of doxorubicin. Therefore, the cytokines released from doxorubicin-stimulated BV2 cells treated with noni had a positive effect on the neuronal viability compared to those released from doxorubicin-stimulated BV2 cells not treated with Noni. Thus, Noni increases neuronal viability. These results suggest that noni inhibits the release of cytokines by regulating the nuclear factor kappa-light-chain-enhancer of the activated B cells pathway of BV2, thereby inhibiting neuronal damage.

Keywords

References

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