Protective effects of aminoethyl-chitooligosaccharides against oxidative stress and inflammation in murine microglial BV-2 cells

被引：13

作者：

Dai-Hung Ngo ^{[2
]}

Dai-Nghiep Ngo ^{[3
]}

Thanh-Sang Vo ^{[2
]}

Ryu, BoMi ^{[1
]}

Quang Van Ta ^{[2
]}

Kim, Se-Kwon ^{[1
]}

机构：

[1] Pukyong Natl Univ, Marine Bioproc Res Ctr, Pusan 608737, South Korea

[2] Pukyong Natl Univ, Dept Chem, Pusan 608737, South Korea

[3] Univ Sci, VNU HCM, Fac Biol, Dept Biochem, Ho Chi Minh City, Vietnam

来源：

CARBOHYDRATE POLYMERS | 2012年 / 88卷 / 02期

关键词：

Aminoethyl-chitooligosaccharides; Murine microglial cells; Antioxidant; Anti-inflammation; Free radicals scavenging; RADICAL-MEDIATED OXIDATION; EXPRESSION; ACTIVATION; DISEASES; INHIBIT; GLIA;

D O I：

10.1016/j.carbpol.2012.01.037

中图分类号：

O69 [应用化学];

学科分类号：

070301 [无机化学];

摘要：

The aim of this study was to investigate the antioxidant and anti-inflammatory activities of aminoethylchitooligosaccharides (AE-COS) in murine microglial cells (BV-2). At the high concentration of 100 mu g/ml, the inhibition of reactive oxygen species. DNA. protein and lipid oxidation were determined in BV-2 cells, at the rates of 77%, 80%, 85% and 85%, respectively. Furthermore, AE-COS was studied for its capabilities against lipopolysaccharide-induced inflammatory responses in BV-2 cells. It was found that AE-COS reduced the level of nitric oxide (NO) and prostaglandin E-2 production by diminishing the expression of inducible NO synthase and cyclooxygenase-2 without significant cytotoxicity. Moreover, the inhibitory activities of AE-COS on generation of tumor necrosis factor-alpha and interleukin-1beta were performed. Collectively, these results indicate that AE-COS possess potential antioxidant and anti-inflammatory activities in brain microglia. and could be a useful therapeutic agent for the treatment of neuroinflammatory diseases. (c) 2012 Elsevier Ltd. All rights reserved.

引用

页码：743 / 747

页数：5

共 20 条

[1]

Arato Endr, 2006, Magy Seb, V59, P50

[2]

Microglia-mediated neurotoxicity: uncovering the molecular mechanisms [J].