文献类型：期刊文献

英文题名：Butyrolactone-I from Coral-Derived Fungus Aspergillus terreus Attenuates Neuro-Inflammatory Response via Suppression of NF-κB Pathway in BV-2 Cells

作者：Zhang, Yuan Yuan[1];Zhang, Yi[1,2];Yao, Yuan-Bei[1];Lei, Xiao-Ling[1];Qian, Zhong-Ji[2,3]

机构：[1]Guangdong Ocean Univ, Coll Food Sci & Technol, Zhanjiang 524088, Peoples R China;[2]Guangdong Ocean Univ, Shenzhen Inst, Shenzhen 518108, Peoples R China;[3]Guangdong Ocean Univ, Coll Chem & Environm, Zhanjiang 524088, Peoples R China

年份：2018

卷号：16

期号：6

外文期刊名：MARINE DRUGS

收录：SCI-EXPANDED(收录号：WOS:000436499000027)、、WOS

基金：The study was supported by the Yangfan Scarce Top Talent Project of Guangdong Province and the Program for Scientific Research Start-up Funds of Guangdong Ocean University (201433008 and 201433009); And supported by Basic Research and Free Exploration Grant of Shenzhen Science and Technology Innovative Committee (JCYJ 20170306165013264) and Department of Science and Technology of Guangdong Province (2013B02100015).

语种：英文

外文关键词：butyrolactone-I; Aspergillus terreus; microglia; neuro-inflammation

外文摘要：Butyrolactone-I (ZB5-1) from the coral-derived fungus Aspergillus terreus was investigated in this study to estimate its anti-neuroinflammatory effects on lipopolysaccharide (LPS)-induced BV-2 microglia cells. MTT assay indicated that ZB5-1 in tested concentrations had no cytotoxicity on BV-2 cells, and significantly reduced the production of nitric oxide (NO), measured using Griess reagent, and interleukin-1 beta (IL-1), detected by enzyme-linked immunosorbent assay (ELISA). ZB5-1 also down-regulated the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in a dose-dependent manner by Western blot analysis. Moreover, the effect of ZB5-1 on the nuclear factor-B (NF-B) signaling pathway was studied via the expression of phosphorylation of NF-B p65 and inhibitor of NF-B (IB), and the nuclear translocation of NF-B p65 respectively. The results showed that ZB5-1 could inhibit the phosphorylation of p65 and IB. Furthermore, molecular docking study suggested that ZB5-1 bound at the active sites of NF-B to prevent its translocation to the nucleus. Therefore, we suggest ZB5-1 has a potential to reduce the anti-inflammatory response in LPS-induced BV-2 cells.