RETRACTED ARTICLE: Effect of catalpol on remyelination through experimental autoimmune encephalomyelitis acting to promote Olig1 and Olig2 expressions in mice

Tao Yang,Qi Zheng,Su Wang,Ling Fang,Lei Liu,Hui Zhao,Lei Wang,Yongping Fan

doi:10.1186/s12906-017-1642-2

Abstract

BackgroundMultiple sclerosis (MS) as an autoimmune disorder is a common disease occurring in central nervous system (CNS) and the remyelination plays a pivotal role in the alleviating neurological impairment in the MS. Catalpol, an effective component extracted from the Chinese herb Radix Rehmanniae, which has been proved protective in cerebral diseases.MethodsTo determine the protective effects and mechanisms of Catalpol on MS, the mice with experimental autoimmune encephalomyelitis (EAE) were induced by myelin oligodendrocyte glycoprotein (MOG) 35–55, as a model for human MS. Th17 cells were counted by flow cytometric (FCM). The expressions of nerve-glial antigen (NG) 2 and myelin basic protein (MBP) were measured by immunohistochemical staining. Olig1+ and Olig2+/BrdU+ cells were counted by immunofluorescence. Olig1 and Olig2 gene expressions were detected by real-time fluorescent quantitative reverse transcription (qRT) -PCR.ResultsThe results showed that Catalpol improved neurological function, reduced inflammatory cell infiltration and demyelination. It could decrease Th17 cells in the peripheral blood. It increased the protein expressions of NG2 and MBP in mice brains, up-regulated markedly protein and gene expressions of Olig1 and Olig2 in terms of timing, site and targets.ConclusionsThese data demonstrated that Catalpol had a strong neuroprotective effect on EAE mice. Catalpol also plays a role in remyelination by promoting the expressions of Olig1 and Olig2 transcription factors.

Highlights

Multiple sclerosis (MS) as an autoimmune disorder is a common disease occurring in central nervous system (CNS) and the remyelination plays a pivotal role in the alleviating neurological impairment in the MS
The study found that MS demyelination following endogenous oligodendrocyte precursor cells (OPCs) repopulate the lesion areas, and which differentiate into mature oligodendrocytes (OLs) to induce OPC-mediated remyelination [7]
Neurological function scores of the mice Neurological impairment was visually apparent from Day 8 and all mice developed neurological deficiencies

Summary

Introduction

Multiple sclerosis (MS) as an autoimmune disorder is a common disease occurring in central nervous system (CNS) and the remyelination plays a pivotal role in the alleviating neurological impairment in the MS. Multiple sclerosis (MS) is characterized by local inflammation, demyelination, gliosis and neuronal destruction through T-cells and macrophages surrounding white matter in the central nervous system (CNS) [1, 2]. These are most responsible for disabilities as a result of neural dysfunction in teenagers [3,4,5].

Methods

Results

Conclusion