Calorie restriction promotes remyelination in a Cuprizone-Induced demyelination mouse model of multiple sclerosis
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ORIGINAL ARTICLE
Calorie restriction promotes remyelination in a Cuprizone-Induced demyelination mouse model of multiple sclerosis Sina Mojaverrostami 1 & Parichehr Pasbakhsh 1 & Soheila Madadi 2 & Saeid Nekoonam 1 & Davood Zarini 1 & Leila Noori 1 & Elham Shiri 1 & Mohamad Salama 3 & Kazem Zibara 4 & Iraj Ragerdi Kashani 1 Received: 4 March 2020 / Accepted: 29 June 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Over the past few decades several attempts have been made to introduce a potential and promising therapy for Multiple sclerosis (MS). Calorie restriction (CR) is a dietary manipulation to reduce calorie intake which has been shown to improve neuroprotection and attenuate neurodegenerative disorders. Here, we evaluated the effect of 33% CR regimen for 4 weeks on the remyelination capacity of Cuprizone (CPZ) induced demyelination in a mouse model of MS. Results showed that CR induced a significant increase in motor coordination and balance performance in CPZ mice. Also, luxol fast blue (LFB) staining showed that CR regimen significantly improved the remyelination in the corpus callosum of CPZ + CR mice compared to the CPZ group. In addition, CR regimen significantly increased the transcript expression levels of BDNF, Sox2, and Sirt1 in the corpus callosum of CPZ mice, while decreasing the p53 levels. Moreover, CR regimen significantly decreased the apoptosis rate. Furthermore, astrogliosis (GFAP + astrocytes) and microgliosis (Iba-1 + microglia) were significantly decreased by CR regimen while oligodendrogenesis (Olig2+) and Sirt1 + cell expression were significantly increased in the corpus callosum of CPZ + CR mice compared to the CPZ group. In conclusion, CR regimen can promote remyelination potential in a CPZ-demyelinating mouse model of MS by increasing oligodendrocyte generation while decreasing their apoptosis. Keywords Calorie restriction . Cuprizone . Demyelination . Multiple sclerosis . Remyelination
Introduction Multiple sclerosis (MS) is a chronic demyelinating disorder of the central nervous system (CNS) (Gharibi et al. 2015; Mojaverrostami et al. 2018). Many scientists agreed to the autoimmune nature for the etiology of MS, however, it is still challenging to give a definite reason for the origins of the disease (Jadidi-Niaragh and Mirshafiey 2011). Destruction and loss of myelin sheaths in the CNS, as well as axonal
* Iraj Ragerdi Kashani [email protected] 1
Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
2
Department of Anatomy, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran
3
Neuroscience Unit, Menoufia Medical School, Shebin El Kom, Egypt
4
ER045, PRASE, DSST and Biology Department, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon
damage are the main pathological hallmarks of MS (Ghasemi et al. 2017). MS can result in different mental and physical problems such as paralysis, ataxia, fatigue visual problems and depression (Halabchi et al. 2017). To date, more than 15
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