c-Jun N-terminal kinase-mediated anti-inflammatory effects of Garcinia subelliptica in macrophages
- Authors
- Cho, Young-Chang; Cho, Sayeon
- Issue Date
- Mar-2016
- Publisher
- SPANDIDOS PUBL LTD
- Keywords
- ethanol extracts of Garcinia subelliptica; nitric oxide; interleukin-6; tumor necrosis factor-; c-Jun N-terminal kinase
- Citation
- MOLECULAR MEDICINE REPORTS, v.13, no.3, pp 2293 - 2300
- Pages
- 8
- Journal Title
- MOLECULAR MEDICINE REPORTS
- Volume
- 13
- Number
- 3
- Start Page
- 2293
- End Page
- 2300
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/7201
- DOI
- 10.3892/mmr.2016.4791
- ISSN
- 1791-2997
1791-3004
- Abstract
- Garcinia plants have been traditionally used to treat inflammatory diseases, such as skin infections and pain, in many regions including South-East Asia. Garcinia subelliptica, a plant of the Garcinia species widely distributed from Japan to Thailand, has been reported to contain components similar to other Garcinia plants that exhibit anti-inflammatory effects. The present study aimed to explore the anti-inflammatory effects of ethanol extracts of Garcinia subelliptica (EGS) in macrophages, as there are no previous systemic studies that have investigated the effects of Garcinia subelliptica on inflammation. Non-cytotoxic concentrations of EGS (200 mu g/ml) were observed to reduce nitric oxide production by modulating iNOS expression in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. The expression of cyclooxygenase-2, the enzyme responsible for the production of prostaglandin E-2, was notably reduced by EGS. EGS treatment inhibited the production of pro-inflammatory cytokines, including IL-6 and IL-1, however, not TNF-. Reduced production of inflammatory mediators by EGS was followed by reduced phosphorylation of c-Jun N-terminal kinase (JNK) however, not of other mitogen-activated protein kinases and nuclear factor-B. These results indicate that EGS selectively inhibits the excessive production of inflammatory mediators in LPS-stimulated murine macrophages by reducing the activation of JNK, suggesting that EGS is a candidate for modulating severe inflammation.
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