Open AccessLeonurine suppresses neuroinflammation through promoting oligodendrocyte maturation
Author(s) -
Jin Min,
Li Qian,
Gu Yuting,
Wan Bing,
Huang Jiefang,
Xu Xuanbai,
Huang Rui,
Zhang Yanyun
Publication year - 2019
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.14053
Subject(s) - remyelination , experimental autoimmune encephalomyelitis , neuroinflammation , multiple sclerosis , myelin oligodendrocyte glycoprotein , oligodendrocyte , microglia , central nervous system , inflammation , immune system , immunology , myelin , biology , neuroscience
Focal inflammation and remyelination failure are major hallmarks of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis ( EAE ). In this study, we found that leonurine, a bioactive alkaloid, alleviated EAE disease severity along with reduced central nervous system inflammation and myelin damage. During the pathogenesis of EAE , leonurine dramatically suppressed the recruitment of encephalitogenic T cells into the central nervous system, whereas did not impair periphery immune responses and microglia activation. Mechanistically, leonurine protected mice against demyelination along with enhanced remyelination through promoting the maturation of oligodendrocytes in both EAE and cuprizone‐induced demyelination mouse models. Moreover, we identified that the expression of demethylase jumonji domain‐containing protein D3 was significantly enhanced upon treatment of leonurine, which suppressed the trimethylation of histone H3 lysine‐27 and enhanced oligodendrocyte maturation accordingly. Collectively, our study identified the therapeutic effect of leonurine on EAE model, which potentially represents a promising therapeutic strategy for multiple sclerosis, even other demyelination disorders.