Salidroside provides neuroprotection by modulating microglial polarization after cerebral ischemia

Xiangrong Liu1,2, Shaohong Wen1,2, Feng Yan2,3

  • 1China-America Institute of Neuroscience, Xuanwu Hospital of Capital Medical University, Beijing, 100053, People's Republic of China.

Abstract

Insights

Salidroside (SLDS) reduces brain damage and improves function after stroke by shifting microglia from a pro-inflammatory (M1) to an anti-inflammatory (M2) state. This modulation promotes oligodendrocyte differentiation and neuronal survival, offering new therapeutic avenues.

Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Microglia play crucial roles in stroke pathology, exhibiting pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes.
  • Salidroside (SLDS) is recognized for its anti-inflammatory and neuroprotective properties, but its specific mechanisms in stroke remain unclear.

Purpose of the Study:

  • To investigate the effects of Salidroside (SLDS) on neuroprotection and microglial polarization following stroke.

Main Methods:

  • Male C57/BL6 mice underwent focal cerebral ischemia and received intravenous SLDS.
  • Microglial polarization was assessed using RT-PCR and immunostaining.
  • Coculture systems evaluated SLDS-induced microglial effects on oligodendrocytes and neurons.

Main Results:

  • SLDS significantly decreased cerebral infarct volume and improved neurological outcomes.
  • SLDS treatment promoted a shift from M1 to M2 microglial polarization, enhancing phagocytosis and reducing inflammatory cytokines.
  • SLDS-treated microglia supported oligodendrocyte differentiation and protected neurons from oxygen-glucose deprivation.

Conclusions:

  • Salidroside (SLDS) demonstrates neuroprotective effects against cerebral ischemia by modulating microglial polarization towards an M2 phenotype.
  • Understanding SLDS-driven microglial polarization mechanisms may reveal novel therapeutic strategies for stroke treatment.

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