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Avicenna Journal of Phytomedicine، جلد ۱۳، شماره ۶، صفحات ۵۹۷-۶۱۴

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عنوان انگلیسی Silibinin effects on cognitive disorders: Hope or treatment?
چکیده انگلیسی مقاله Objective: Almost all diseases of the nervous system are related to neuroinflammation, oxidative stress, neuronal death, glia activation, and increased pro-inflammatory cytokines. Cognitive disorders are one of the common complications of nervous system diseases. The role of some plant compounds in reducing or preventing cognitive disorders has been determined. Silibinin is a plant bioflavonoid and exhibits various effects on cognitive functions. This article discusses the different mechanisms of the effect of silibinin on cognitive disorders in experimental studies.Materials and Methods: Databases, including ISI, , Google Scholar, Scopus, Medline and PubMed, were investigated from 2000 to 2021, using related keywords to find required articles.Results: Silibinin can improve cognitive disorders by different pathways such as reducing neuroinflammation and oxidative stress, activation of reactive oxygen species- Brain-derived neurotrophic factor- Tropomyosin receptor kinase B (ROS–BDNF–TrkB) pathway in the hippocampus, an increase of dendritic spines in the brain, inhibition of hyperphosphorylation of tau protein and increasing the expression of insulin receptor (IR) and insulin-like growth factor receptor 1 (IGF-1R), inhibiting inflammatory responses and oxidative stress in the hippocampus and amygdala, and decrease of Homovanillic acid/Dopamine (HVA/DA) ratio and 3,4-Dihydroxyphenylacetic acid + Homovanillic acid/Dopamine (DOPAC+ HVA/DA) ratio in the prefrontal cortex and 5-hydroxyindoleacetic acid/5-hydroxytryptamine (5-HIAA/5-HT) ratio in the hippocampus.Conclusion: These results suggest that silibinin can be considered a therapeutic agent for the symptom reduction of cognitive disorders, and it acts by affecting various mechanisms such as inflammation, programmed cell death, and oxidative stress.
کلیدواژه‌های انگلیسی مقاله Silibinin, Cognitive disorders, Neuroinflammation, Oxidative stress

نویسندگان مقاله | Zahra Akhoond-Ali
Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran


| Alireza Rahimi
Material Science and Metallurgy Engineering, Karaj Branch, Islamic Azad University, Karaj, Iran


| Atiyeh Ghorbani
Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran


| Fatemeh Forouzanfar
Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Neuroscience, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran


| Sara Hosseinian
Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran


| Hamed Ghazavi
Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran


| Farzaneh Vafaee
Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Department of Neuroscience, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran



نشانی اینترنتی https://ajp.mums.ac.ir/article_21959.html
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