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从海洋海绵Phorbas sp.中分离出的Phorbaketal A，通过抑制脂多糖刺激的巨噬细胞中的NF-κB和激活血红素加氧酶-1发挥其抗炎作用。

Phorbaketal A, Isolated from the Marine Sponge Phorbas sp., Exerts Its Anti-Inflammatory Effects via NF-κB Inhibition and Heme Oxygenase-1 Activation in Lipopolysaccharide-Stimulated Macrophages.

作者信息

Seo Yun-Ji, Lee Kyung-Tae, Rho Jung-Rae, Choi Jung-Hye

机构信息

Department of Life & Nanopharmaceutical Sciences, Kyung Hee University, Seoul 130-701, Korea.

College of Pharmacy, Kyung Hee University, Seoul 130-701, Korea.

出版信息

Mar Drugs. 2015 Nov 19;13(11):7005-19. doi: 10.3390/md13117005.

DOI:10.3390/md13117005
PMID:26610528
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4663563/
Abstract

Marine sponges harbor a range of biologically active compounds. Phorbaketal A is a tricyclic sesterterpenoid isolated from the marine sponge Phorbas sp.; however, little is known about its biological activities and associated molecular mechanisms. In this study, we examined the anti-inflammatory effects and underlying molecular mechanism of phorbaketal A in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. We found that phorbaketal A significantly inhibited the LPS-induced production of nitric oxide (NO), but not prostaglandin E₂, in RAW 264.7 cells. Further, phorbaketal A suppressed the expression of inducible NO synthase at both the mRNA and protein levels. In addition, phorbaketal A reduced the LPS-induced production of inflammatory cytokines such as tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6, and monocyte chemotactic protein-1. Treatment with phorbaketal A inhibited the transcriptional activity of nuclear factor-kappaB (NF-κB), a crucial signaling molecule in inflammation. Moreover, phorbaketal A up-regulated the expression of heme oxygenase-1 (HO-1) in LPS-stimulated RAW 264.7 cells. These data suggest that phorbaketal A, isolated from the marine sponge Phorbas sp., inhibits the production of inflammatory mediators via down-regulation of the NF-κB pathway and up-regulation of the HO-1 pathway.

摘要

海洋海绵含有一系列生物活性化合物。佛波贝酮A是一种从海洋海绵Phorbas sp.中分离出的三环倍半萜；然而，对其生物活性和相关分子机制知之甚少。在本研究中，我们检测了佛波贝酮A对脂多糖（LPS）刺激的RAW 264.7巨噬细胞的抗炎作用及其潜在分子机制。我们发现，佛波贝酮A显著抑制RAW 264.7细胞中LPS诱导的一氧化氮（NO）生成，但不抑制前列腺素E₂的生成。此外，佛波贝酮A在mRNA和蛋白质水平上均抑制诱导型NO合酶的表达。另外，佛波贝酮A减少了LPS诱导的炎症细胞因子如肿瘤坏死因子-α、白细胞介素（IL）-1β、IL-6和单核细胞趋化蛋白-1的生成。用佛波贝酮A处理可抑制核因子-κB（NF-κB）的转录活性，NF-κB是炎症中的关键信号分子。此外，佛波贝酮A上调了LPS刺激的RAW 264.7细胞中血红素加氧酶-1（HO-1）的表达。这些数据表明，从海洋海绵Phorbas sp.中分离出的佛波贝酮A通过下调NF-κB途径和上调HO-1途径来抑制炎症介质的生成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ffa/4663563/69412d1028dd/marinedrugs-13-07005-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ffa/4663563/71ea1d66237d/marinedrugs-13-07005-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ffa/4663563/2b64ae81d779/marinedrugs-13-07005-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ffa/4663563/04c6f954d855/marinedrugs-13-07005-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ffa/4663563/f4f387bd6a02/marinedrugs-13-07005-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ffa/4663563/69412d1028dd/marinedrugs-13-07005-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ffa/4663563/71ea1d66237d/marinedrugs-13-07005-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ffa/4663563/2b64ae81d779/marinedrugs-13-07005-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ffa/4663563/04c6f954d855/marinedrugs-13-07005-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ffa/4663563/f4f387bd6a02/marinedrugs-13-07005-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ffa/4663563/69412d1028dd/marinedrugs-13-07005-g005.jpg

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