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THU0074 Vitamin e uncouples joint inflammation and articular destruction, in a transgenic mouse model of rheumatoid arthritis
  1. MJ De Bandt1,
  2. F Driss1,
  3. M Grossin1,
  4. J Pincemail2,
  5. C Babin-Chevaye1,
  6. C Gaertner3,
  7. C Pasquier1
  1. 1INSERM U 479, Bichat, Paris, France
  2. 2CHU de Liège, Domaine Du Start Tilman, Liège, Belgique
  3. 3COGNIS, Dusseldorf, Deutschland

Abstract

Background Reactive oxygen species (ROS) are suspected to play a role in human RA. Transient hypoxia and ischaemic-reperfusion phenomenon are involved in their chronic production, by monocytes and macrophages. Nevertheless the clinical interest of ROS scavengers is difficult to evaluate.

Methods We studied the effects of Vitamin E (natural alpha tocopherol) on transgenic KRN/NOD mice, new model for rheumatoid arthritis. We determined clinical, histological and biochemical parameters so as to define the long-term benefit of Vitamin E in the disease.

Results We found an increase in plasma Vit E, in treated mice. Vitamin E treatment did not modify the date of onset of the disease, neither the intensity of the disease (arthritic index and weight), but Vit-E prevented from articular destruction, suggesting uncoupling of the two phenomenon. Biochemical analysis, blood glutathion, urine isoprostane and the plasma hydroperoxide did not differ between Vit E-treated transgenic KRN/NOD mice and control mice. Blood chemiluminescence was increased in transgenic KRN/NOD mice as compared to non-transgenic mice, and was decreased in Vit E-treated transgenic KRN/NOD mice. TNF-a and IL1-b, low in control non-transgenic mice, were increased in transgenic KRN/NOD mice, however a significant decreased in IL-1b appeared in Vit E-treated mice.

Conclusion These results suggest that ROS scavengers can modulate cytokines responses and provide new arguments for the interest of ROS scavengers in RA therapy.

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