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Int Immunopharmacol. 2019 Oct;75:105777. doi: 10.1016/j.intimp.2019.105777. Epub 2019 Jul 26.

Cordycepin (3'-deoxyadenosine) promotes remyelination via suppression of neuroinflammation in a cuprizone-induced mouse model of demyelination.

Author information

1
State Key Laboratory for Conservation and Utilization of Bio-resources in Yunnan, Yunnan University, Kunming 650091, Yunnan, China; Yunnan University, School of Medicine, 2 Cuihu North Road, Kunming 650091, Yunnan, China.
2
The National Clinical Research Center for Mental Disorders, Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Capital Medical University, Beijing 100088, China.
3
Yunnan University, The School of Life Sciences, 2 Cuihu North Road, Kunming 650091, Yunnan, China.
4
State Key Laboratory for Conservation and Utilization of Bio-resources in Yunnan, Yunnan University, Kunming 650091, Yunnan, China; Yunnan University, School of Medicine, 2 Cuihu North Road, Kunming 650091, Yunnan, China. Electronic address: dujing@ynu.edu.cn.

Abstract

Multiple sclerosis (MS) is an inflammatory demyelination disease characterized by autoimmune damage to the central nervous system. In this disease, failure of remyelination could cause persistent disability. Cordycepin, also known as 3'-deoxyadenosine, exerts anti-inflammatory, anti-oxidic, anti-apoptotic and neuroprotective effects. The cuprizone (CPZ) model has been widely used to study MS as it mimics some characteristics of demyelination disease. To determine whether cordycepin promotes remyelination and functional recovery after CPZ-induced demyelination, we administered cordycepin to the CPZ-induced demyelination mice. Cordycepin reversed CPZ-induced loss of body weight and rescued motor dysfunction in the model mice. Cordycepin effectively promoted remyelination and enhanced MBP expression in the corpus callosum. Cordycepin also inhibited the CPZ-induced increase in the number of Iba1-positive microglia, GFAP-positive astrocytes and Olig2-positive oligodendroglial precursor cells in the corpus callosum and cerebral cortex. Pro-inflammatory cytokine expression (IL-1β and IL-6) was inhibited while anti-inflammatory cytokine IL-4 and neurotrophic factor BDNF release was elevated in the corpus callosum and hippocampus after cordycepin treatment. In addition, we also found that cordycepin ameliorated CPZ-induced body weight loss, motor dysfunction, demyelination, glial cells activation and pro-inflammatory cytokine expression in the corpus callosum and hippocampus. Our results suggest that cordycepin may represent a useful therapeutic agent in demyelination-related diseases via suppression of neuroinflammation.

KEYWORDS:

Astrocytes; Cordycepin; Microglia; Multiple sclerosis; Oligodendrocytes; Remyelination

PMID:
31357085
DOI:
10.1016/j.intimp.2019.105777
[Indexed for MEDLINE]

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