Open AccessEffect of 1.25(OH)2D3 on experimental autoimmune neuritis and its mechanism
Author(s) -
Di Nian,
Zhuohan Li,
Jie Sun,
Peng Shi
Publication year - 2021
Publication title -
trends in immunotherapy
Language(s) - English
Resource type - Journals
ISSN - 2573-5985
DOI - 10.24294/ti.v5.i2.1.1375
Subject(s) - medicine , neuritis , pathological , vitamin d and neurology , foxp3 , myelin , endocrinology , pathology , immunology , immune system , central nervous system , surgery
Objective: To study the potential therapeutic effects of active vitamin D3 (1.25(OH)2D3) in the experimental autoimmune neuritis (EAN). Methods: The EAN model was established by actively immunizing Lewis rats with synthetic P0180–199 pepide and Freund’s complete adjuvant. 1.25(OH)2D3 treatment was given, weight change of rats and clinical score were analyzed. HE staining was used to detect the inflammatory cell infiltration of sciatic nerves and demyelination of sciatic nerves was observed by transmission electron microscope (TEM) at the same time. The expressions of inflammatory cytokines IL-17, IL-10, TGF-β, IFN-γ were detected by ELISA, and the expressions of Th17, Treg were examined by RT-PCR. Results: 1.25(OH)2D3 ameliorated body weight loss and myelin lesions. It decreased expressions of inflammatory cytokines IL-17, IFN-γ and RORrt while those of IL-10, TGF-β and FoxP3 were increased. Conclusions: 1.25(OH)2D3 can improve the clinical pathological changes of EAN rats, and the mechanism may be related to the changes of inflammatory cytokines. 1.25(OH)2D3 is expected to become a new strategy for the clinical treatment of GBS/EAN.