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Pentoxifylline inhibits experimental allergic encephalomyelitis
S Nataf1, J P Louboutin, D Chabannes
1Clinique Neurologique, Hopital Laënnec, C.H.R.U. Nantes, France.
Abstract:
Pentoxifylline, a widely used methylxanthine, has been proven to inhibit the production and action of the cytokine TNF alpha. Since it has been suggested that TNF alpha is the major cytokine involved in the pathogenesis of multiple sclerosis, we tested pentoxifylline for its capacity to prevent experimental allergic encephalomyelitis (EAE). 26 Lewis rats with acute EAE were treated with either pentoxifylline or saline. The pentoxifylline treated rats showed a significantly lower incidence of clinical signs as well as significantly lower histological inflammation. The exact mechanism of this preventive effect remains to be clarified but it might be mainly related to inhibition of TNF alpha release from central nervous system macrophages.
Insights
Pentoxifylline, a methylxanthine, reduced the incidence and severity of experimental allergic encephalomyelitis (EAE) in rats. This suggests pentoxifylline may be a potential therapeutic agent for multiple sclerosis by inhibiting tumor necrosis factor alpha.
Area of Science:
- Neuroimmunology
- Pharmacology
Background:
- Tumor necrosis factor alpha (TNF alpha) is implicated in the pathogenesis of multiple sclerosis (MS).
- Pentoxifylline is a methylxanthine known to inhibit TNF alpha production and action.
Purpose of the Study:
- To investigate the potential of pentoxifylline in preventing experimental allergic encephalomyelitis (EAE), an animal model for MS.
Main Methods:
- 26 Lewis rats with acute EAE were administered either pentoxifylline or a saline control.
- Clinical signs and histological inflammation were assessed.
Main Results:
- Pentoxifylline treatment resulted in a significantly lower incidence of clinical signs of EAE.
- Histological examination revealed significantly reduced inflammation in pentoxifylline-treated rats compared to controls.
Conclusions:
- Pentoxifylline demonstrated a preventive effect against EAE in rats.
- The mechanism may involve the inhibition of TNF alpha release from central nervous system macrophages, suggesting a potential therapeutic role in MS.