Journal of Microbiology and Biotechnology

The Korean Society for Microbiology and Biotechnology (한국미생물·생명공학회)
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The Aqueous Extract of Radio-Resistant Deinococcus actinosclerus BM2T Suppresses Lipopolysaccharide-Mediated Inflammation in RAW264.7 Cells

  • Kim, Myung Kyum (Department of Bio & Environmental Technology, College of Natural Science, Seoul Women's University) ;
  • Jang, Seon-A (Herbal Medicine Research Division, Korea Institute of Oriental Medicine) ;
  • Namkoong, Seung (College of Health Sciences, Kangwon National University) ;
  • Lee, Jin Woo (College of Health Sciences, Kangwon National University) ;
  • Park, Yuna (Department of Bio & Environmental Technology, College of Natural Science, Seoul Women's University) ;
  • Kim, Sung Hyeok (College of Health Sciences, Kangwon National University) ;
  • Lee, Sung Ryul (Department of Convergence Biomedical Science, Cardiovascular and Metabolic Disease Center, College of Medicine, Inje University) ;
  • Sohn, Eun-Hwa (College of Health Sciences, Kangwon National University)
  • Received : 2019.11.04
  • Accepted : 2019.12.14
  • Published : 2020.04.28
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Abstract

Deinococcus actinosclerus BM2T (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 BM2T 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 BM2T, on lipopolysaccharide (LPS)-mediated inflammatory responses in RAW264.7 macrophage cells. BM2U showed antioxidant capacity, as determined by the DPPH radical scavenging (IC50 = 349.3 ㎍/ml) and ORAC (IC50 = 50.24 ㎍/ml) assays. At 20 ㎍/ml, BM2U induced a significant increase in heme oxygenase-1 (HO-1) expression (p < 0.05). BM2U treatment (0.2-20 ㎍/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.

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References

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