Vitamin E uncouples joint destruction and clinical inflammation in a transgenic mouse model of rheumatoid arthritis
| Autor: | Catherine Pasquier, Fathi Driss, Michel De Bandt, M. Grossin, Joël Pincemail, C. Babin-Chevaye |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Antioxidant
medicine.medical_treatment Immunology Arthritis Mice Transgenic Inflammation Isoprostanes Pharmacology Antioxidants Arthritis Rheumatoid Mice Rheumatology Mice Inbred NOD Leukocytes medicine Animals Vitamin E Immunology and Allergy Pharmacology (medical) NOD mice Tumor Necrosis Factor-alpha business.industry Body Weight Zymosan Hydrogen Peroxide medicine.disease Glutathione Disease Models Animal Cytokine Rheumatoid arthritis Luminescent Measurements Joints Tumor necrosis factor alpha medicine.symptom business Oxidation-Reduction Interleukin-1 |
| Zdroj: | Arthritis & Rheumatism. 46:522-532 |
| ISSN: | 1529-0131 0004-3591 |
| DOI: | 10.1002/art.10085 |
| Popis: | Objective Reactive oxygen species are thought to play a role in rheumatoid arthritis (RA) in humans. We postulated that antioxidant treatment could have a beneficial effect in this disease. We therefore investigated the effects of vitamin E in the transgenic KRN/NOD mouse model of RA. Methods Mice were treated by gavage with oral vitamin E (α-tocopherol). Clinical, histologic, and biochemical parameters were assessed for 6 weeks. Results Vitamin E treatment did not modify the clinical features of the disease (date of onset or disease intensity, as measured by the articular index), but it did prevent joint destruction, as measured by qualitative and semiquantitative analyses. Redox status did not differ between treated and control mice. White blood cell chemiluminescence was higher in transgenic KRN/NOD mice than in controls, but vitamin E treatment attenuated this difference. Vitamin E treatment of the transgenic animals led to a significant decrease in the levels of interleukin-1β (IL-1β) but not tumor necrosis factor α. Conclusion Vitamin E seems to uncouple joint inflammation and joint destruction in this model of RA, with a beneficial effect on joint destruction. Since many investigations are currently in progress to evaluate the benefit of interventions targeted toward anti-IL-1β, our findings suggest opportunities of therapeutic interest in human RA. |
| Databáze: | OpenAIRE |
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