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KMID : 0624620090420060380
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BMB Reports
2009 Volume.42 No. 6 p.380 ~ p.386
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NSA9, a human prothrombin kringle-2-derived peptide, acts as an inhibitor of kringle-2-induced activation in EOC2 microglia
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Kim Ji-Yeon
Kim Tae-Hyong
Kim Soung-Soo
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Abstract
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In neurodegenerative diseases, such as Alzheimer’s and Parkinson’s, microglial cell activation is thought to contribute to CNS injury by producing neurotoxic compounds. Prothrombin and kringle-2 increase levels of NO and the mRNA expression of iNOS, IL-1β, and TNF-α in microglial cells. In contrast, the human prothrombin kringle-2 derived peptide NSA9 inhibits NO release and the production of pro-inflammatory cytokines such as IL-1β, TNF-α, and IL-6 in LPS-activated EOC2 microglia. In this study, we investigated the anti-inflammatory effects of NSA9 in human prothrombin- and kringle-2-stimulated EOC2 microglia. Treatment with 20-100 μM of NSA9 attenuated both prothrombin- and kringle-2-induced microglial activation. NO production induced by MAPKs and NF-κB was similarly reduced by inhibitors of ERK (PD98059), p38 (SB203580), NF-κB (N-acetylcysteine), and NSA9. These results suggest that NSA9 acts independently as an inhibitor of microglial activation and that its effects in EOC2 microglia are not influenced by the presence of kringle-2.
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KEYWORD
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Human prothrombin kringle-2, MAPKs (mitogen-activated protein kinases), Microglia, NF-κB (nuclear factor-kappa B), NSA9
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