Alpha-tocopherol ameliorates experimental autoimmune encephalomyelitis through the regulation of Th1 cells

Document Type : Original Article

Authors

1 Department of Clinical Laboratory, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450002, China

2 Key Clinical Laboratory Medicine of Henan Province, Zhengzhou 450002, China

3 Department of Laboratory Medicine, Zhengzhou University, Zhengzhou, Henan 450002, China

4 Key Laboratory of the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan450002, China

Abstract

Objective(s): Multiple sclerosis (MS) is a serious neurological autoimmune disease, it commonly affects young adults. Vitamin E (Vit E) is an important component of human diet with antioxidant activity, which protects the body’s biological systems. In order to assess the effect of Vit E treatment on this autoimmune disease, we established experimental autoimmune encephalomyelitis (EAE), the animal model of MS, and treated EAE with α-tocopherol (AT) which is the main content of Vit E.
Materials and Methods:Twenty C57BL/6 adult female mice were used and divided into two groups randomly. EAE was induced with myelin oligodendrocyte glycoprotein (MOG), and one group was treated with AT, at a dose of 100 mg/kg on the 3th day post-immunization with MOG, the other group was treated with 1% alcohol. Mice were euthanized on day 14, post-immunization, spleens were removed for assessing splenocytes proliferation and cytokine profile, and spinal cords were dissected to assess the infiltration of inflammatory cells in spinal cord.
Results:AT was able to attenuate the severity of EAE and delay the disease progression. H&E staining and fast blue staining indicated that AT reduced the inflammation and the demyelination reaction in the spinal cord. Treatment with AT significantly decreased the proliferation of splenocytes. AT also inhibited the production of IFN-γ (Th1 cytokine), though the other cytokines were only affected slightly.
Conclusion:According to the results, AT ameliorated EAE, through suppressing the proliferation of T cells and the Th1 response. AT may be used as a potential treatment for MS.

Keywords

References

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Iranian Journal of Basic Medical Sciences
Volume 19, Issue 5
May 2016
Pages 561-566

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