The marine-derived furanone reduces intracellular lipid accumulation in vitro by targeting LXR alpha and PPAR alpha
文献类型：期刊论文
| 作者 | Li, Ting; Hu, Shu-Mei; Pang, Xiao-Yan; Wang, Jun-Feng; Yin, Jia-Yu; Li, Fa-Hui; Wang, Jin; Yang, Xiao-Qian; Xia, Bin; Liu, Yong-Hong |
| 刊名 | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
 |
| 出版日期 | 2020 |
| 卷号 | 24期号:6页码:3384 |
| ISSN号 | 1582-1838 |
| 关键词 | acetyl-CoA carboxylase fatty acid synthase furanone LXR antagonist PPAR antagonist PPAR alpha agonist reverse cholesterol transport |
| DOI | 10.1111/jcmm.15012 |
| 英文摘要 | Recent studies have demonstrated that commercially available lipid-lowering drugs cause various side effects; therefore, searching for anti-hyperlipidaemic compounds with lower toxicity is a research hotspot. This study was designed to investigate whether the marine-derived compound, 5-hydroxy-3-methoxy-5-methyl-4-butylfuran-2(5H)-one, has an anti-hyperlipidaemic activity, and the potential underlying mechanism in vitro. Results showed that the furanone had weaker cytotoxicity compared to positive control drugs. In RAW 264.7 cells, the furanone significantly lowered ox-LDL-induced lipid accumulation (50%), and its triglyceride (TG)-lowering effect was greater than that of liver X receptor (LXR) agonist T0901317. In addition, it significantly elevated the protein levels of peroxisome proliferator-activated receptors (PPAR alpha) and ATP-binding cassette (ABC) transporters, which could be partially inhibited by LXR antagonists, GSK2033 and SR9243. In HepG2 cells, it significantly decreased oleic acid-induced lipid accumulation, enhanced the protein levels of low-density lipoprotein receptor (LDLR), ABCG5, ABCG8 and PPAR alpha, and reduced the expression of sterol regulatory element-binding protein 2 (32%). PPAR alpha antagonists, GW6471 and MK886, could significantly inhibit the furanone-induced lipid-lowering effect. Furthermore, the furanone showed a significantly lower activity on the activation of the expression of lipogenic genes compared to T0901317. Taken together, the furanone exhibited a weak cytotoxicity but had powerful TC- and TG-lowering effects most likely through targeting LXR alpha and PPAR alpha, respectively. These findings indicate that the furanone has a potential application for the treatment of dyslipidaemia. |
| 资助机构 | National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [31300639, 81770463]; Shandong Provincial Natural Science FundNatural Science Foundation of Shandong Province [ZR2013HQ014] ; National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [31300639, 81770463]; Shandong Provincial Natural Science FundNatural Science Foundation of Shandong Province [ZR2013HQ014] |
| 源URL | [http://ir.scsio.ac.cn/handle/344004/18509]  |
| 专题 | 南海海洋研究所_中科院海洋生物资源可持续利用重点实验室 |
| 作者单位 | 1.[Li, Ting 2.Pang, Xiao-Yan 3.Hu, Shu-Mei 4.Chinese Acad Sci, CAS Key Lab Trop Marine Bioresources & Ecol, South China Sea Inst Oceanol, Guangdong Key Lab Marine Mat Med,RNAM Ctr Marine, Guangzhou 510220, Peoples R China 5.[Wang, Jun-Feng 6.Weifang Med Univ, Innovat Drug Res Ctr, Sch Pharm, Inst Lipid Metab & Atherosclerosis, Weifang 261053, Peoples R China 7.Song, Wei-Guo 8.Xia, Bin 9.Yang, Xiao-Qian 10.Wang, Jin |
| 推荐引用方式 GB/T 7714 | Li, Ting,Hu, Shu-Mei,Pang, Xiao-Yan,et al. The marine-derived furanone reduces intracellular lipid accumulation in vitro by targeting LXR alpha and PPAR alpha[J]. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE,2020,24(6):3384, 3398. |
| APA | Li, Ting.,Hu, Shu-Mei.,Pang, Xiao-Yan.,Wang, Jun-Feng.,Yin, Jia-Yu.,...&Guo, Shou-Dong.(2020).The marine-derived furanone reduces intracellular lipid accumulation in vitro by targeting LXR alpha and PPAR alpha.JOURNAL OF CELLULAR AND MOLECULAR MEDICINE,24(6),3384. |
| MLA | Li, Ting,et al."The marine-derived furanone reduces intracellular lipid accumulation in vitro by targeting LXR alpha and PPAR alpha".JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 24.6(2020):3384. |
入库方式： OAI收割
来源：南海海洋研究所
浏览0
下载0
收藏0
其他版本
除非特别说明，本系统中所有内容都受版权保护，并保留所有权利。