Amelioration of experimental autoimmune encephalomyelitis by Ishige okamurae.
10.5115/acb.2018.51.4.292
- Author:
Meejung AHN
1
;
Jeongtae KIM
;
Wonjun YANG
;
Yuna CHOI
;
Poornima EKANAYAKE
;
Hyunju KO
;
Youngheun JEE
;
Taekyun SHIN
Author Information
1. Department of Veterinary Anatomy, Veterinary Medical Research Institute, College of Veterinary Medicine, Jeju National University, Jeju, Korea. shint@jejunu.ac.kr
- Publication Type:Original Article
- Keywords:
Experimental autoimmune encephalomyelitis;
Inflammation;
Ishige okamurae;
Spinal cord
- MeSH:
Animals;
Central Nervous System;
Cyclooxygenase 2;
Encephalomyelitis, Autoimmune, Experimental*;
Ethanol;
Inflammation;
Myelin Basic Protein;
Necrosis;
Oxidative Stress;
Paralysis;
Rats;
Spinal Cord;
Spleen;
T-Lymphocytes
- From:Anatomy & Cell Biology
2018;51(4):292-298
- CountryRepublic of Korea
- Language:English
-
Abstract:
Experimental autoimmune encephalomyelitis (EAE) is a T-cell-mediated autoimmune central nervous system disease characterized by inflammation with oxidative stress. The aim of this study was to evaluate an anti-inflammatory effect of Ishige okamurae on EAE-induced paralysis in rats. An ethanolic extract of I. okamurae significantly delayed the first onset and reduced the duration and severity of hind-limb paralysis. The neuropathological and immunohistochemical findings in the spinal cord were in agreement with these clinical results. T-cell proliferation assay revealed that the ethyl-acetate fraction of I. okamurae suppressed the proliferation of myelin basic protein reactive T cells from EAE affected rats. Flow cytometric analysis showed TCRαβ+ T cells was significantly reduced in the spleen of EAE rats with I. okamurae treatment with concurrent decrease of inflammatory mediators including tumor necrosis factor-α and cyclooxygenase-2. Collectively, it is postulated that I. okamurae ameliorates EAE paralysis with suppression of T-cell proliferation as well as decrease of pro-inflammatory mediators as far as rat EAE is concerned.
