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Suppression of Inducible Nitric Oxide Synthase and cyclooxygenase-2 by Cell-Permeable Superoxide Dismutase in Lipopolysaccharide-Stimulated BV-2 Microglial Cells

Suppression of Inducible Nitric Oxide Synthase and cyclooxygenase-2 by Cell-Permeable Superoxide Dismutase in Lipopolysaccharide-Stimulated BV-2 Microglial Cells

Ji Ae Lee, Ha Yong Song, Sung Mi Ju, Su Jin Lee, Won Yong Seo, Dong Hyeon Sin, Ah Ra Goh, Soo Young Choi, Jinseu Park

Mol Cells. 2010 Mar;29(3):245-50.

PMID: 20108167

Abstract:

Oxidative stress plays a pivotal role in uncontrolled neuro-inflammation leading to many neurological diseases including Alzheimer's. One of the major antioxidant enzymes known to prevent deleterious effects due to oxidative stress is Cu,Zn-superoxide dismutase (SOD). In this study, we examined the regulatory function of SOD on the LPS-induced signaling pathways leading to NF-kappaB activation, expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), in BV-2 cells using cell-permeable SOD. Treatment of BV-2 cells with cell-permeable SOD led to a decrease in LPS-induced reactive oxygen species (ROS) generation and significantly inhibited protein and mRNA levels of iNOS and COX-2 upregulated by LPS. Production of NO and PGE2 in LPS stimulated BV-2 cells was significantly abrogated by pretreatment with a cell-permeable SOD fusion protein. Furthermore, cell-permeable SOD inhibited LPS-induced NF-kappaB DNA-binding activity and activation of MAP kinases including ERK, JNK, and p38 in BV-2 cells. These data indicate that SOD has a regulatory function for LPS-induced NF-kappaB activation leading to expression of iNOS and COX-2 in BV-2 cells and suggest that cell-permeable SOD is a feasible therapeutic agent for regulation of ROS-related neurological diseases.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42415483	ERK Activation Inhibitor Peptide II, Cell-Permeable			Price

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