Ginsenoside Rb1 attenuates mouse cerebral ischemia/reperfusion induced neurological impairments through modulation of

Cong Yu1, Yisong Zhang1, Yijun Guo1

  • 1Department of Neurosurgery, the People's Hospital of Shanghai Pudong New Area, Shanghai, China.

Folia Neuropathologica
|August 21, 2024
PubMed

Insights

Ginsenoside Rb1 (GS-Rb1) protects the brain from stroke damage by reducing neurological deficits and anxiety. This neuroprotective effect is achieved by regulating microglia polarization, shifting from harmful M1 to beneficial M2 types.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Pathology

Background:

  • Cerebral ischemia/reperfusion leads to significant disability and mortality.
  • Microglia activation is a key response to ischemic stroke.
  • Ginsenoside Rb1 (GS-Rb1) shows potential neuroprotective properties in the central nervous system.

Purpose of the Study:

  • To investigate the neuroprotective effects of GS-Rb1 against cerebral ischemia/reperfusion.
  • To evaluate GS-Rb1's impact on neurological function, anxiety, and cognitive impairment.
  • To explore GS-Rb1's influence on microglial activation and polarization.

Main Methods:

  • A middle cerebral artery occlusion (MCAO) mouse model was employed.
  • GS-Rb1 was administered intraperitoneally at doses of 5, 10, or 20 mg/kg.
  • Neurological function (mNSS), anxiety (open field test), and cognition (Morris water maze) were assessed.
  • Protein and mRNA levels were analyzed using ELISA, Western blot, and qRT-PCR.

Main Results:

  • GS-Rb1 treatment significantly reduced modified neurological severity scoring (mNSS) and brain water content.
  • GS-Rb1 alleviated cognitive impairment and anxiety-like behaviors.
  • GS-Rb1 inhibited overall microglial activation, promoting M2 polarization and suppressing M1 polarization.

Conclusions:

  • GS-Rb1 demonstrates significant neuroprotective effects in a mouse model of cerebral ischemia/reperfusion.
  • GS-Rb1 ameliorates neurological deficits, cognitive impairment, and anxiety.
  • The neuroprotective mechanism involves the regulation of microglia polarization from M1 to M2 phenotypes.

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