JS-III-49, a hydroquinone derivative, exerts anti-inflammatory activity by targeting Akt and p38
- Authors
- Yi, Young-Su; Kim, Mi-Yeon; Cho, Jae Youl
- Issue Date
- May-2017
- Publisher
- KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
- Keywords
- Akt; Anti-inflammatory activity; HQ derivative; JS-III-49; Macrophages; p38
- Citation
- KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, v.21, no.3, pp.345 - 352
- Journal Title
- KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
- Volume
- 21
- Number
- 3
- Start Page
- 345
- End Page
- 352
- URI
- http://scholarworks.bwise.kr/ssu/handle/2018.sw.ssu/6385
- DOI
- 10.4196/kjpp.2017.21.3.345
- ISSN
- 1226-4512
- Abstract
- Since previous studies have reported that hydroquinone (HQ) exerted immunosuppressive and anti-inflammatory activity, various HQ derivatives have been synthesized and their biological activities investigated. In this study, we explored the anti-inflammatory activity of JS-III-49, a novel HQ derivative, in macrophage mediated inflammatory responses. JS-III-49 suppressed the production of the inflammatory mediators nitric oxide (NO) and prostaglandin E-2, (PGE(2)) and down regulated the mRNA expression of the inflammatory enzymes cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) as well as the expression of the pro-inflammatory cytokines interleukin-6 (IL-6) and IL-1 beta without cytotoxicity in LPS-stimulated RAW264.7 cells. JS-III-49 inhibited nuclear translocation of the NF-kappa B transcription factors p65 and p50 by directly targeting Akt, an upstream kinase of the NF-kappa B pathway, in LPS-stimulated RAW264.7 cells. However, JS-III-49 did not directly inhibit the kinase activities of Src and Syk, which are upstream kinases of Akt, in LPS-stimulated RAW264.7 cells. Moreover, JS-III-49 suppressed the nuclear translocation of c-Fos, one of the components of AP-1, by specifically targeting p38, an upstream mitogen-activated protein kinase (MAPK) in the AP-1 pathway in LPS-stimulated RAW264.7 cells. These results suggest that JS-III-49 plays an anti-inflammatory role in LPS-stimulated macrophages by targeting Akt and p38 in the NF-kappa B and AP-1 pathways, respectively.
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