Macrolactins from Marine-Derived Bacillus subtilis B5 Bacteria as Inhibitors of Inducible Nitric Oxide and Cytokines Expression.
Macrolactins from Marine-Derived Bacillus subtilis B5 Bacteria as Inhibitors of Inducible Nitric Oxide and Cytokines Expression.
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DOI：
10.3390/md14110195
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发表时间：
2016-10-26
期刊：
影响因子：
5.4
通讯作者：
Qiu YK
中科院分区：
文献类型：
--
作者：
Yan X;Zhou YX;Tang XX;Liu XX;Yi ZW;Fang MJ;Wu Z;Jiang FQ;Qiu YK
为寻找具有抗炎活性的天然产物，对一株3000 m深海沉积物来源的枯草芽孢杆菌B5进行了化学成分研究。分离并鉴定了一种新的大环内酯衍生物7，13-epoxyl-macrolactin A（1）。由于环氧环的存在，与先前分离的已知大环内酯相比，1对诱导型一氧化氮和细胞因子的表达表现出显著的抑制作用（2-5）。实时聚合酶链反应（PCR）分析显示，新化合物显著抑制脂多糖（LPS）刺激的RAW 264.7巨噬细胞中诱导型一氧化氮合酶（iNOS）、白细胞介素-1 β（IL-1β）和白细胞介素-6（IL-6）的mRNA表达。逆转录-PCR分析表明，新化合物以浓度依赖性方式降低IL-1β的mRNA表达水平。
In order to find new natural products with anti-inflammatory activity, chemical investigation of a 3000-meter deep-sea sediment derived bacteria Bacillus subtilis B5 was carried out. A new macrolactin derivative was isolated and identified as 7,13-epoxyl-macrolactin A (1). Owing to the existence of the epoxy ring, 1 exhibited a significant inhibitory effect on the expression of inducible nitric oxide and cytokines, compared with previously isolated known macrolactins (2–5). Real-time Polymerase Chain Reaction (PCR) analysis showed that the new compound significantly inhibited the mRNA expressions of inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Reverse transcription-PCR analysis demonstrated that the new compound reduced the mRNA expression level of IL-1β in a concentration-dependent manner.
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影响因子：
5.1
作者：
Mondol, M. A. Mojid;Tareq, Fakir Shahidullah;Shin, Hee Jae
通讯作者：
Shin, Hee Jae
影响因子：
78.8
作者：
Crusz, Shanthini M.;Balkwill, Frances R.
通讯作者：
Balkwill, Frances R.
影响因子：
5.4
作者：
Robertson RC;Guihéneuf F;Bahar B;Schmid M;Stengel DB;Fitzgerald GF;Ross RP;Stanton C
通讯作者：
Stanton C
影响因子：
4.4
作者：
Kurakula, Kondababu;Vos, Mariska;de Vries, Carlie J. M.
通讯作者：
de Vries, Carlie J. M.
影响因子：
15
作者：
GUSTAFSON, K;ROMAN, M;FENICAL, W
通讯作者：
FENICAL, W