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Updated: Jun 5, 2026
Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis
Published on: September 9, 2022
Fibrinogen depleting agent batroxobin has a beneficial effect on experimental autoimmune encephalomyelitis
Yang Yang1, Shu-juan Tian, Lei Wu
1Department of Neurology, The General Hospital of Chinese PLA, Beijing, China. cuteyyang@gmail.com
Abstract:
Multiple sclerosis (MS) was characterized with widespread demyelination and axonal loss of central nervous system (CNS). Fibrinogen (fibrin) deposition was considered as one of the pathogenesis of MS. Therefore, we explored the effects of fibrinogen depleting agent batroxobin in experimental autoimmune encephalomyelitis (EAE) mice model. Our study showed that prevention and suppression with batroxobin significantly ameliorated clinical severity of EAE, reduced inflammatory cells infiltration, and demyelination, and suppressed the activation of astrocytes and macrophages comprising the CD11b(+) population. Batroxobin treatment leads to reduced expression of p-Akt and increased expression of MBP as compared to control. In addition, batroxobin treatment partly reversed the dendric-like formation of macrophages irritated by fibrinogen in vitro. The reduced severity of EAE mice treated with batroxobin suggests that strategy targeting fibrin as a potential therapy for EAE may be beneficial for the treatment of MS patients.
Insights
Batroxobin, a fibrinogen-depleting agent, effectively reduced multiple sclerosis (MS) symptoms in a mouse model by decreasing inflammation and demyelination. This suggests targeting fibrin may be a promising therapeutic strategy for MS patients.
Area of Science:
- Neuroscience
- Immunology
Background:
- Multiple sclerosis (MS) involves central nervous system (CNS) demyelination and axonal loss.
- Fibrinogen (fibrin) deposition is implicated in MS pathogenesis.
Purpose of the Study:
- To investigate the therapeutic potential of batroxobin, a fibrinogen-depleting agent, in a mouse model of MS (experimental autoimmune encephalomyelitis - EAE).
Main Methods:
- Administration of batroxobin in the EAE mouse model.
- Assessment of clinical severity, inflammatory cell infiltration, demyelination, and glial cell activation (astrocytes and macrophages).
- In vitro evaluation of batroxobin's effect on fibrinogen-irritated macrophages.
Main Results:
- Batroxobin treatment significantly reduced EAE clinical severity.
- Reduced inflammatory cell infiltration, demyelination, and suppressed astrocyte/macrophage activation were observed.
- Batroxobin decreased p-Akt expression and increased myelin basic protein (MBP) expression.
- In vitro, batroxobin reversed fibrinogen-induced macrophage morphological changes.
Conclusions:
- Targeting fibrin with agents like batroxobin shows therapeutic promise for EAE.
- This approach may offer a beneficial strategy for treating multiple sclerosis in humans.
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