THE EFFECT OF CANABIDIOL TO ATTENUATES AUTOPHAGY MARKERS IN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS MODEL OF MULTIPLE SCLEROSIS
Publish place: 13th annual international addiction science congress
Publish Year: 1398
نوع سند: مقاله کنفرانسی
زبان: English
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شناسه ملی سند علمی:
KAMED13_031
تاریخ نمایه سازی: 10 دی 1398
Abstract:
Background and Aim : Neurodegenerative diseases are including a large group of conditions associated with progressive neuronal loss. Multiple sclerosis (MS) is a demyelinating autoimmune disease which experimental autoimmune encephalomyelitis (EAE) is a suitable model to study its pathogenesis. Also, Autophagy plays an important role in maintaining the cellular homeostasis, is involved in the mechanisms of neuronal damage during MS. Ablation of autophagy leads to neurodegeneration and Autophagy is tightly linked to the innate and adaptive immune systems during the autoimmune process, and several studies have shown that autophagy directly participates in the progress of MS or EAE. Therefore Autophagy might be a therapeutic strategy for MS. Methods : Marijuana (Cannabinoids) has been shown to exhibit potent anti-inflammatory properties and have been shown to be effective in the treatment of a number of autoimmune diseases, including MS. Cannabidiol (CBD) is a non-psychotomimetic and phytocannabinoid derived from Cannabis sativa. Beneficial effects and neuroprotection properties of CBD have been described in a wide range of psychiatric disorders, including anxiety, psychosis and depression. CBD exhibits a broad spectrum of potential therapeutic properties in animal models and humans, including, anxiolytic, antidepressant, neuroprotective, anti-inflammatory and immunomodulatoryResults : We will emphasize the neuroprotective, anti-inflammatory, and immunomodulatory benefits of CBD on neurodegenerative disease. Therapeutic effects of CBD, focusing on their relevance to brain function, neuroprotection and neuropsychiatric disordersConclusion : In this review, we discuss the role of CBD on autophagy markers in the neuroinflammation and neurodegeneration associated with the pathogenesis of EAE.
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Authors
Maryam Akhavan tavakoli matak
Department of Medical Basic Sciences, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran
Maryam Soleimani
Department of Anatomy, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
Mehdi Mehdizadeh
Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran
Azam Govahi
Department of Anatomy, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran