eISSN: 1509-572x
ISSN: 1641-4640
Folia Neuropathologica
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3/2023
vol. 61
 
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abstract:
Original paper

Astragaloside IV inhibits experimental autoimmune encephalomyelitis by modulating the polarization of both microglia/macrophages and astrocytes

Jingwen Yu
1
,
Bingtao Mu
1
,
Minfang Guo
1
,
Chunyun Liu
1
,
Tao Meng
1
,
Yuqing Yan
1
,
Lijuan Song
2
,
Jiezhong Yu
2
,
Gajendra Kumar
3
,
Cungen Ma
2

  1. Institute of Brain Science, Shanxi Key Laboratory of Inflammatory Neurodegenerative Diseases, Shanxi Datong University, China
  2. The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine, Research Center of Neurobiology, Shanxi University of Chinese Medicine, China
  3. Department of Neuroscience, City University of Hong Kong, Tat Chee Avenue, Kowloon, Hong Kong
Folia Neuropathol 2023; 61 (3): 273-290
Online publish date: 2023/07/04
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Astragaloside IV (AST IV), a major saponin component and active ingredient isolated from Astragalus membranaceus, has been well known to exhibit neuroprotective effects on diverse models of neurological diseases. Accumulating evidence suggests that dynamic balance of microglia/macrophages and astrocytes plays a vital role in neuroprotection and remyelination. However, dysregulation of microglia/macrophages and astrocytes orchestrate the pathogenesis of nervous system disorders. Therefore, we hypothesized that switching the transformation of microglia/macrophages and astrocytes into the neuroprotective M2 and A2 phenotypes, respectively, could be a potential target for therapeutic intervention.

In the present study, we evaluate the efficacy of AST IV intervention on the effects of microglia/macrophages and astrocytes in an experimental autoimmune encephalomyelitis (EAE) model. AST IV improved paralysis and pathology of EAE by inhibiting the neurotoxic M1 microglia/macrophage phenotype, promoting M2 phenotype, shifting astrocytes towards a neuroprotective A2 phenotype, and protecting neurons from apoptosis through inhibition of TLR4/Myd88/NF-kB signalling pathway. Our study showed that AST IV could be a potential and promising drug for multiple sclerosis treatment.
keywords:

experimental autoimmune encephalomyelitis (EAE), microglial, macrophages, astrocytes

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