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Inhibitory Effects of Glycoprotein Isolated from Laminaria japonica on Lipopolysaccharide‐Induced Pro‐Inflammatory Mediators in BV2 Microglial Cells
Author(s) -
Park HyeYoung,
Han MinHo,
Kim GiYoung,
Kim Nam Deuk,
Nam TaekJeong,
Choi Yung Hyun
Publication year - 2011
Publication title -
journal of food science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 150
eISSN - 1750-3841
pISSN - 0022-1147
DOI - 10.1111/j.1750-3841.2011.02287.x
Subject(s) - microglia , proinflammatory cytokine , nitric oxide , lipopolysaccharide , tumor necrosis factor alpha , p38 mitogen activated protein kinases , chemistry , protein kinase b , nitric oxide synthase , neuroprotection , microbiology and biotechnology , prostaglandin e , pharmacology , kinase , protein kinase a , signal transduction , inflammation , immunology , biology , biochemistry , organic chemistry
Chronic microglial activation endangers neuronal survival through release of various toxic pro‐inflammatory molecules; therefore, negative regulators of microglial activation have been identified as potential therapeutic candidates for use in treatment of many neurological diseases. In this study, we conducted an investigation of the inhibitory effects of glycoprotein isolated from Laminaria japonica (LJGP) on production of lipopolysaccharide (LPS)‐induced pro‐inflammatory mediators in BV2 microglial cells. Data from the study indicated that treatment with LJGP resulted in significant inhibition of excessive production of nitric oxide and prostaglandin E 2 in LPS‐stimulated BV2 cells. LJGP also attenuated expression of inducible nitric oxide synthase, cyclooxygenase‐2, and pro‐inflammatory cytokines, including interleukin‐1β and tumor necrosis factor‐α. In addition, LJGP exhibited anti‐inflammatory properties by suppression of nuclear factor‐kappaB activation and downregulation of extracellular signal‐regulated kinase, p38 mitogen‐activated protein kinase, and Akt pathways. These findings suggest LJGP may provide neuroprotection through suppression of the proinflammatory pathway in activated microglia.