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Plant-based product Apigenin attenuates EAE severity through the modulation of immune cell function (THER7P.948)
Journal article   Peer reviewed

Plant-based product Apigenin attenuates EAE severity through the modulation of immune cell function (THER7P.948)

Rashida Ginwala, Emily McTish, Divya Sagar, Chander Raman, Pooja Jain and Zafar Khan
The Journal of immunology (1950), v 194(1_Supplement), pp 208-208.8
01 May 2015
DOI: https://doi.org/10.4049/jimmunol.194.Supp.208.8

Abstract

Abstract The use of Apigenin, a naturally occurring plant flavone, for centuries to treat asthma, Parkinson's disease, neuralgia, and shingles, indicates its importance in the regulation of inflammation. However, its effect on dendritic cells (DC) that maintain the critical balance between an immunogenic and tolerogenic immune response especially in neuroinflammation is relatively unknown. To test if Apigenin treatment ameliorates disease after onset of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, C57BL/6 mice immunized with MOG35-55 were treated with Apigenin. A significant reduction in severity of EAE progression was observed in the treated mice with disease peak lasting only a day. Splenocytes isolated from Apigenin treated EAE mice show decreased expression of α4 integrin and increased DCs and macrophages compared to untreated EAE mice. This correlated with immunohistochemistry findings of decreased immune cell infiltration and reduced demyelination in the CNS. In vitro, Apigenin inhibited TNF-α and IL-6 secretion in mice splenic DCs stimulated with LPS and the cell surface expression of MHC II and CD86 molecules on bone marrow derived DCs. These results indicate a protective role of Apigenin against the neurodegenerative effects resulting from the entry of DC stimulated pathogenic T cells into the CNS. Apigenin can thus serve as a potential therapy for neuroinflammatory disease through its regulation of immunogenic T cell response.

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