Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/10711
Title: The beneficial effects of 18ß-glycyrrhetinic acid on the experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mouse model
Authors: Kamışlı, S.
Çiftçi, Osman
Taşlıdere, A.
Başak Türkmen, N.
Özcan, C.
Keywords: 18ß-glycyrrhetinic acid
C57BL/6
EAE
multiple sclerosis
TNF-alpha
caspase 3
glycyrrhetinic acid
interleukin 17
interleukin 1beta
tumor necrosis factor
18alpha-glycyrrhetinic acid
Casp3 protein, mouse
cytokine
animal experiment
animal model
Article
biochemical analysis
brain tissue
clinical feature
controlled study
experimental autoimmune encephalomyelitis
female
histology
histopathology
lipid peroxidation
mouse
nonhuman
oxidative stress
priority journal
analogs and derivatives
animal
brain
chemically induced
drug effect
metabolism
pathology
Animals
Brain
Caspase 3
Cytokines
Encephalomyelitis, Autoimmune, Experimental
Female
Glycyrrhetinic Acid
Lipid Peroxidation
Mice
Oxidative Stress
Publisher: Taylor and Francis Ltd
Abstract: Aim: The aim of this study was to investigate the beneficial effects of 18ß-glycyrrhetinic acid (GA) on the experimental allergic encephalomyelitis (EAE) in C57BL/6 mice. GA is a natural substance found in the root of licorice and is used in traditional Chinese medicine. It has many pharmacological activities such as antioxidant, anti-inflammatory, and anti-cancer effects. Materials and methods: A total of 40 C57BL/6 mice were divided equally into four groups: (1) Control, (2) EAE, (3) GA and (4) GA + EAE. 14 days after induction of EAE with MOG35-55 and pertussis toxin, mice were treated with GA at doses of 100 mg/kg/day for 7 days intraperitoneally. Results: To our results, oxidative stress and lipid peroxidations (elevated TBARS levels, decreased GPx, SOD, CAT, and GSH levels) were significantly (p <.01) increased, causing EAE in brain tissue. Also, histopathological damage (Caspase-3 and IL-17 activity, p ?.01) and cytokine levels (TNF-? and IL-1ß, p <.01) were induced with EAE in mice brain tissue. On the other hand, GA treatment significantly (p <.01) reversed oxidative histological and immunological alterations caused by EAE. Conclusions: In conclusion, the GA treatment can protect the brain tissue against EAE in mice with its antioxidant and anti-inflammatory properties. © 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group.
URI: https://hdl.handle.net/11499/10711
https://doi.org/10.1080/08923973.2018.1490318
ISSN: 0892-3973
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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