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The Aqueous Extract of Radio-Resistant Deinococcus actinosclerus BM2T Suppresses Lipopolysaccharide-Mediated Inflammation in RAW264.7 Cells
Deinococcus actinosclerus BM2(T) (GenBank: KT448814) is a radio-resistant bacterium that is newly isolated from the soil of a rocky hillside in Seoul. As an extremophile, D. actinosclerus BM2(T) may possess anti-inflammatory properties that may be beneficial to human health. In this study, we evalua...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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The Korean Society for Microbiology and Biotechnology
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9728386/ https://www.ncbi.nlm.nih.gov/pubmed/31838828 http://dx.doi.org/10.4014/jmb.1911.11003 |
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author | Kim, Myung Kyum Jang, Seon-A Namkoong, Seung Lee, Jin Woo Park, Yuna Kim, Sung Hyeok Lee, Sung Ryul Sohn, Eun-Hwa |
author_facet | Kim, Myung Kyum Jang, Seon-A Namkoong, Seung Lee, Jin Woo Park, Yuna Kim, Sung Hyeok Lee, Sung Ryul Sohn, Eun-Hwa |
author_sort | Kim, Myung Kyum |
collection | PubMed |
description | Deinococcus actinosclerus BM2(T) (GenBank: KT448814) is a radio-resistant bacterium that is newly isolated from the soil of a rocky hillside in Seoul. As an extremophile, D. actinosclerus BM2(T) may possess anti-inflammatory properties that may be beneficial to human health. In this study, we evaluated the anti-inflammatory effects of BM2U, an aqueous extract of D. actinosclerus BM2(T), on lipopolysaccharide (LPS)-mediated inflammatory responses in RAW264.7 macrophage cells. BM2U showed antioxidant capacity, as determined by the DPPH radical scavenging (IC(50) = 349.3 μg/ml) and ORAC (IC(50) = 50.24 μg/ml) assays. At 20 μg/ml, BM2U induced a significant increase in heme oxygenase-1 (HO-1) expression (p < 0.05). BM2U treatment (0.2-20 μg/ml) significantly suppressed LPS-induced increase in the mRNA expression of proinflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 (p < 0.05). BM2U treatment also suppressed the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), which are involved in the production of inflammatory mediators. BM2U treatment also inhibited the activation of nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs): JNK, ERK, and p-38 (p < 0.05). Collectively, BM2U exhibited anti-inflammatory potential that can be exploited in attenuating inflammatory responses. |
format | Online Article Text |
id | pubmed-9728386 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | The Korean Society for Microbiology and Biotechnology |
record_format | MEDLINE/PubMed |
spelling | pubmed-97283862022-12-13 The Aqueous Extract of Radio-Resistant Deinococcus actinosclerus BM2T Suppresses Lipopolysaccharide-Mediated Inflammation in RAW264.7 Cells Kim, Myung Kyum Jang, Seon-A Namkoong, Seung Lee, Jin Woo Park, Yuna Kim, Sung Hyeok Lee, Sung Ryul Sohn, Eun-Hwa J Microbiol Biotechnol Research article Deinococcus actinosclerus BM2(T) (GenBank: KT448814) is a radio-resistant bacterium that is newly isolated from the soil of a rocky hillside in Seoul. As an extremophile, D. actinosclerus BM2(T) may possess anti-inflammatory properties that may be beneficial to human health. In this study, we evaluated the anti-inflammatory effects of BM2U, an aqueous extract of D. actinosclerus BM2(T), on lipopolysaccharide (LPS)-mediated inflammatory responses in RAW264.7 macrophage cells. BM2U showed antioxidant capacity, as determined by the DPPH radical scavenging (IC(50) = 349.3 μg/ml) and ORAC (IC(50) = 50.24 μg/ml) assays. At 20 μg/ml, BM2U induced a significant increase in heme oxygenase-1 (HO-1) expression (p < 0.05). BM2U treatment (0.2-20 μg/ml) significantly suppressed LPS-induced increase in the mRNA expression of proinflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 (p < 0.05). BM2U treatment also suppressed the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), which are involved in the production of inflammatory mediators. BM2U treatment also inhibited the activation of nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs): JNK, ERK, and p-38 (p < 0.05). Collectively, BM2U exhibited anti-inflammatory potential that can be exploited in attenuating inflammatory responses. The Korean Society for Microbiology and Biotechnology 2020-04-28 2019-12-15 /pmc/articles/PMC9728386/ /pubmed/31838828 http://dx.doi.org/10.4014/jmb.1911.11003 Text en Copyright© 2020 by The Korean Society for Microbiology and Biotechnology https://creativecommons.org/licenses/by/4.0/This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research article Kim, Myung Kyum Jang, Seon-A Namkoong, Seung Lee, Jin Woo Park, Yuna Kim, Sung Hyeok Lee, Sung Ryul Sohn, Eun-Hwa The Aqueous Extract of Radio-Resistant Deinococcus actinosclerus BM2T Suppresses Lipopolysaccharide-Mediated Inflammation in RAW264.7 Cells |
title | The Aqueous Extract of Radio-Resistant Deinococcus actinosclerus BM2T Suppresses Lipopolysaccharide-Mediated Inflammation in RAW264.7 Cells |
title_full | The Aqueous Extract of Radio-Resistant Deinococcus actinosclerus BM2T Suppresses Lipopolysaccharide-Mediated Inflammation in RAW264.7 Cells |
title_fullStr | The Aqueous Extract of Radio-Resistant Deinococcus actinosclerus BM2T Suppresses Lipopolysaccharide-Mediated Inflammation in RAW264.7 Cells |
title_full_unstemmed | The Aqueous Extract of Radio-Resistant Deinococcus actinosclerus BM2T Suppresses Lipopolysaccharide-Mediated Inflammation in RAW264.7 Cells |
title_short | The Aqueous Extract of Radio-Resistant Deinococcus actinosclerus BM2T Suppresses Lipopolysaccharide-Mediated Inflammation in RAW264.7 Cells |
title_sort | aqueous extract of radio-resistant deinococcus actinosclerus bm2t suppresses lipopolysaccharide-mediated inflammation in raw264.7 cells |
topic | Research article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9728386/ https://www.ncbi.nlm.nih.gov/pubmed/31838828 http://dx.doi.org/10.4014/jmb.1911.11003 |
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