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The Aqueous Extract of Radio-Resistant Deinococcus actinosclerus BM2T Suppresses Lipopolysaccharide-Mediated Inflammation in RAW264.7 Cells.
Journal of Microbiology and Biotechnology ( IF 2.8 ) Pub Date : 2019-12-16 , DOI: 10.4014/jmb.1911.11003
Myung Kyum Kim 1 , Seon-A Jang 2, 3 , Seung Namkoong 3 , Jin Woo Lee 3 , Yuna Park 1 , Sung Hyeok Kim 3 , Sung Ryul Lee 4 , Eun-Hwa Sohn 3
Affiliation  

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 μg/ml) and ORAC (IC50 = 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.

中文翻译:

抗辐射放线异常球菌 BM2T 的水提取物抑制 RAW264.7 细胞中脂多糖介导的炎症。

Deinococcus actinosclerus BM2 T (GenBank: KT448814) 是一种抗辐射细菌,新近从首尔岩石山坡的土壤中分离出来。作为极端微生物,D. actinosclerus BM2 T可能具有可能有益于人类健康的抗炎特性。在这项研究中,我们评估了 BM2U(一种D. actinosclerus BM2 T的水提取物)对脂多糖 (LPS) 介导的 RAW264.7 巨噬细胞炎症反应的抗炎作用。BM2U 显示出抗氧化能力,由 DPPH 自由基清除 (IC 50 = 349.3 μg/ml) 和 ORAC (IC 50= 50.24 微克/毫升)测定。在 20 μg/ml 时,BM2U 诱导血红素加氧酶 1 (HO-1) 表达显着增加 ( p < 0.05)。BM2U 处理 (0.2-20 μg/ml) 显着抑制 LPS 诱导的促炎细胞因子肿瘤坏死因子-α (TNF-α)、白细胞介素 (IL)-1β 和 IL-6 的 mRNA 表达增加 ( p < 0.05) . BM2U 治疗还抑制了参与炎症介质产生的诱导型一氧化氮合酶 (iNOS) 和环氧合酶 2 (COX-2) 的表达。BM2U 治疗还抑制了核因子-κB (NF-κB) 和丝裂原活化蛋白激酶 (MAPK) 的激活:JNK、ERK 和 p-38(p< 0.05)。总的来说,BM2U 表现出抗炎潜力,可用于减弱炎症反应。
更新日期:2020-08-21
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