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JCR 2016
جستجوی مقالات
چهارشنبه 26 آذر 1404
Cell Journal
، جلد ۲۴، شماره ۱۱، صفحات ۶۸۱-۶۸۸
عنوان فارسی
چکیده فارسی مقاله
کلیدواژههای فارسی مقاله
عنوان انگلیسی
Ferulic Acid Ameliorates Cell Injuries, Cognitive and Motor Impairments in Cuprizone-Induced Demyelination Model of Multiple Sclerosis
چکیده انگلیسی مقاله
Objective:
Ferulic acid (FA) is a phenolic compound that exhibits neuroprotective effects in the central nervous system
(CNS). This study was conducted to evaluate the potential effects of FA on the cognitive and motor impairments in the
cuprizone-induced demyelination model of multiple sclerosis (MS).
Materials and Methods
:
In this experimental study, demyelination was induced in mice by feeding them with chow
containing cuprizone (CPZ) 0.2% for 6 weeks. Mice in the control group received normal chow. Mice in the CPZ+Veh,
CPZ+FA10, and CPZ+FA100 groups received saline, and FA at a dose of 0, 10, or 100 mg/kg (intraperitoneal, I.P., daily)
respectively. After cognitive and motor assessments, under anaesthesia, animal brains were removed for evaluating
the histological, apoptosis, and molecular changes.
Results:
The results showed that FA increased freezing behaviour in contextual (P<0.05) and cued freezing tests
(P<0.05). FA also reduced the random arm entrance (P<0.01) and increased spontaneous alternations into the arms of
Y-maze compared to the CPZ+Veh group (P<0.05). Time on the rotarod was improved in rats that received both doses
of FA (P<0.01). Demyelination, apoptosis, and relative mRNA expression of p53 were lower in the FA-treated groups
relative to the CPZ+Veh group (P<0.01). In addition, FA increased mRNA expression of brain-derived neurotrophic
factor (Bdnf), Olig2, and Mbp (P<0.05) but decreased GFAP mRNA expression compared to the CPZ+Veh group
(P<0.01).
Conclusion:
The results of this study showed that FA plays a significant neuroprotective role in CPZ models of
demyelination by reducing neuronal apoptosis and improving oligodendrocytes (OLs) growth and differentiation.
کلیدواژههای انگلیسی مقاله
Apoptosis, Cuprizone, Demyelination, Ferulic acid, Oligodendrocyte
نویسندگان مقاله
Mojtaba Ghobadi |
Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
Babak Arji |
Department of Anatomical Sciences, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
Maryam Yadegari |
Department of Anatomical Sciences, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
Mansour Esmailidehaj |
Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
Farshad Homayouni Moghadam |
Department of Animal Biotechnology, Cell Science Research Centre, Royan Institute for Biotechnology, Isfahan, Iran
Mohammad Ebrahim Rezvani |
Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
نشانی اینترنتی
https://www.celljournal.org/article_253347_aa86575cd3263832f3e2ea315ef100de.pdf
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