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Hydroxychloroquine effects on miR-155-3p and miR-219 expression changes in animal model of multiple sclerosis
Abstract
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system which causes chronic demyelination. Hydroxychloroquine (HCQ) possess immunosuppressive and anti-inflammatory properties. The aim of this study was to investigate the effect of HCQ on miR-219 and miR-155-3p expression changes in MS-induced model. The animal model was induced by the administration of cuprizone containing food pellets (0.2%). Briefly, C57BL/6 mice were randomly divided into five groups. Group 1 received normal food and water during the study. Group 2 received cuprizone pellets for 5 weeks (demyelination phase) following one-week normal feeding during the remyelination phase. The remaining three groups received HCQ (2.5, 10 and 100 mg/kg) via drinking water during the demyelination phase. At the end of each phase, mice were deeply anesthetized, perfused with PBS through the heart, and their brains were removed. Brain sections stained with luxol fast blue and the images were analyzed. Also, the expression levels of miR-219 and miR-155-3p were evaluated by quantitative Real-Time PCR in all samples. HCQ decreased the expression of miR-155-3p and increased miR-219 expression in animals treated with 100 mg/kg of HCQ compared to the control group (p < 0.0001) and the cuprizone group (p < 0.0001). LFB method revealed a gradual increment of myelination in animals treated with 10 and 100 mg/kg of HCQ compared to the cuprizone group. Based on the obtained results of this study, HCQ can…
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Downregulation of miR-155-3p may enhance remyelination in MS.
“Their results showed that downregulation of miR-155-3p may enhance remyelination in MS (Mazloumfard et al. 2020).”
From MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis (2025) · cites this paper as Mazloumfard et al. 2020
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Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned
Gudi, V., Gingele, S., Skripuletz, T., & Stangel, M. (2014) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2014.00073 · Cited by 375 · cited 1×
“…prior studies, demyelination in mice fed with 0.2% cuprizone was observed from the second week of treatment and after 5 weeks (phase I), when cuprizone treatment was stopped, the process of demyelination ceased and allowing myelination to return (Phase II) (Lindner et al. 2008; Gudi et al. 2014).”
BackgroundInfluentialGonzález, H., Elgueta, D., Montoya, A., & Pacheco, R. (2014) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2014.07.012 · Cited by 352
miR-219 Cooperates with miR-338 in Myelination and Promotes Myelin Repair in the CNS
Wang, H., Moyano, A. L., Ma, Z., Deng, Y., Lin, Y., Zhao, C., Zhang, L., Jiang, M., He, X., Ma, Z., et al. (2017) · Developmental Cell · doi:10.1016/j.devcel.2017.03.001 · Cited by 174 · cited 1×
“It was observed that the increment of miR-219 and miR-338 expression could increase oligodendrocytes production (Zhao et al. 2010; Wang et al. 2017).”
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MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis
Asl, E. R., Hosseini, S. E., Tahmasebi, F., Bolandi, N., & Barati, S. (2025) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-025-01578-6 · Cited by 19
Metadata
- Authors
- Mazloumfard, F., Mirian, M., Eftekhari, S.-M., & Aliomrani, M.
- Venue
- Metabolic Brain Disease
- Published
- 2020-08-29
- Volume
- 35
- Issue
- 8
- Pages
- 1299-1307
- ISSN
- 0885-7490
- 1573-7365
- Cited by
- 19
- References
- 6
- Language
- en
- Funders
- Isfahan University of Medical Sciences (297133)
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