2. Academic Validation
  3. Calycosin regulates astrocyte reactivity and astrogliosis after spinal cord injury by targeting STAT3 phosphorylation

Calycosin regulates astrocyte reactivity and astrogliosis after spinal cord injury by targeting STAT3 phosphorylation

  • J Neuroimmunol. 2025 Jan 30:400:578535. doi: 10.1016/j.jneuroim.2025.578535.
Wenhai Tang 1,  Aitao Wang 2,  Shengxing Liu 1,  Guangyu Wen 1,  Hao Qi 1,  Yuntao Gu 1,  Chunzhao Xu 1,  Shanwu Ren 1,  Shunli Zhang 3,  Yongxiong He 4
Affiliations

Affiliations

  • 1 Department of Spine Surgery, The Second Affiliated Hospital of Hainan Medical University, Haikou 570216, China.
  • 2 Department of Anesthesiology, Hohhot First Hospital, Hohhot 010030, China.
  • 3 Department of Spine Surgery, The Second Affiliated Hospital of Hainan Medical University, Haikou 570216, China. Electronic address: zsl18976362357@126.com.
  • 4 Department of Orthopedics, Beijing Chest Hospital, Capital Medical University, Beijing 101149, China. Electronic address: spinedoctor@sina.com.
PMID: 39954615 DOI: 10.1016/j.jneuroim.2025.578535
Abstract

Background: Astrocytes are the most populous glial cells in the central nervous system (CNS), which can exert detrimental effects through a process of reactive astrogliosis. Our previous study has indicated the potential effect of Calycosin in preventing spinal cord injury (SCI). This study aims to investigate the mechanism by which calycosin regulates the polarization of A1 astrocytes, a neurotoxic subtype of reactive astrocytes, in SCI models.

Materials and methods: The SCI model was induced by applying mechanical compression to the spinal cord using vascular clamps. A1 astrocyte differentiation was induced by treating astrocytes with microglia supernatant obtained after Lipopolysaccharide (LPS) stimulation. Key protein expression levels were analyzed by Western blotting, and astrocyte markers such as CS56, GFAP, C3, S100A10 were assessed through immunofluorescence staining.

Results: Calycosin treatment significantly reduced glial scar formation and C3 expression in SCI rats. However, S100A10 expression remained unchanged. Further analysis showed that Calycosin inhibited A1 astrocyte activation, migration, and invasion, which was associated with STAT3 phosphorylation. Calycosin downregulated p-STAT3 levels in both A1 astrocytes and SCI rats. These effects were reversed by Colivelin (a STAT3 Activator) in A1 astrocytes.

Conclusion: Calycosin treatment can modulate p-STAT3 expression, thereby altering the functionality of astrocytes during the recovery phase and positively impacting the treatment and rehabilitation of SCI.

Keywords

A1 astrocytes; Calycosin; P-STAT3; Reactive astrogliosis; Spinal cord injury.

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