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Mol. Cells 2010; 29(3): 245-250

Published online March 31, 2010

https://doi.org/10.1007/s10059-010-0031-1

© The Korean Society for Molecular and Cellular Biology

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

Ji Ae Lee1,3, Ha Yong Song1,3, Sung Mi Ju1, Su Jin Lee1, Won Yong Seo1, Dong Hyeon Sin1, Ah Ra Goh1, Soo Young Choi1,2, and Jinseu Park1,2,*

1Department of Biomedical Science and Medical and Bio-material Research Center Hallym University, Chunchon 200-702, Korea, 2Research Institute for Bioscience and Biotechnology, College of Natural Sciences, Hallym University, Chunchon 200-702, Korea, 3These authors contributed equally to this work.

Correspondence to : *Correspondence: jinpark@hallym.ac.kr

Received: July 6, 2009; Revised: November 27, 2009; Accepted: November 27, 2009

Abstract

Oxidative stress plays a pivotal role in uncontrolled neu-roinflammation leading to many neurological diseases including Alzheimer’s. One of the major antioxidant en-zymes 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 up-regulated 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.

Keywords COX-2, iNOS, LPS, NF-κB, ROS, superoxide dismutase

Article

Research Article

Mol. Cells 2010; 29(3): 245-250

Published online March 31, 2010 https://doi.org/10.1007/s10059-010-0031-1

Copyright © The Korean Society for Molecular and Cellular Biology.

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

Ji Ae Lee1,3, Ha Yong Song1,3, Sung Mi Ju1, Su Jin Lee1, Won Yong Seo1, Dong Hyeon Sin1, Ah Ra Goh1, Soo Young Choi1,2, and Jinseu Park1,2,*

1Department of Biomedical Science and Medical and Bio-material Research Center Hallym University, Chunchon 200-702, Korea, 2Research Institute for Bioscience and Biotechnology, College of Natural Sciences, Hallym University, Chunchon 200-702, Korea, 3These authors contributed equally to this work.

Correspondence to:*Correspondence: jinpark@hallym.ac.kr

Received: July 6, 2009; Revised: November 27, 2009; Accepted: November 27, 2009

Abstract

Oxidative stress plays a pivotal role in uncontrolled neu-roinflammation leading to many neurological diseases including Alzheimer’s. One of the major antioxidant en-zymes 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 up-regulated 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.

Keywords: COX-2, iNOS, LPS, NF-κB, ROS, superoxide dismutase

Mol. Cells
Nov 30, 2022 Vol.45 No.11, pp. 763~867
COVER PICTURE
Naive (cyan) and axotomized (magenta) retinal ganglion cell axons in Xenopus tropicalis (Choi et al., pp. 846-854).

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