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Radioresistant Deinococcus Actinosclerus BM2 T Suppresses Lipopolysaccharide‐mediated Inflammation in the RAW264.7 Cells
Author(s) -
Park Yuna,
Jang Seon-A,
Lee Jin Woo,
Kim Sung Hyeok,
Ha Chang Woo,
Lee Sung Ryul,
Kim Myung Kyum,
Sohn Eun-Hwa
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.00744
Subject(s) - proinflammatory cytokine , lipopolysaccharide , tumor necrosis factor alpha , radioresistance , p38 mitogen activated protein kinases , inflammation , chemistry , nitric oxide synthase , nitric oxide , mapk/erk pathway , kinase , microbiology and biotechnology , biology , immunology , biochemistry , cell culture , genetics , organic chemistry
Deinococcus actinosclerus BM2 T (designated to KT448814) is newly isolated radioresistant bacterium from soil of a rocky hillside. As an extremophile, D. actinosclerus BM2 T may express health‐beneficial compounds for combating inflammation. In this study, we evaluated anti‐inflammatory potentials of BM2W, a water extract of D. actinosclerus BM2 T , on lipopolysaccharide (LPS)‐mediated inflammatory responses in the RAW264.7 macrophages. LPS‐induced mRNA expression levels of proinflammatory cytokines, such as interleukin (IL)‐1β, IL‐6 and tumor necrosis factor‐α, were significantly inhibited in the presence of BM2W. Inductions of inflammatory mediator producing inducible nitric oxide synthase and cyclooxygenase‐2 proteins were also suppressed by BM2W treatment. BM2W led inhibition of activation of nuclear factor‐κB and mitogen‐activated protein kinases (JNK, ERK and p38). Collectively, BM2W seems to be potent in attenuating inflammatory responses via MAPKs/NF‐κB pathway.