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An ethyl-acetate fraction of Holothuria scabra modulates inflammation in vitro through inhibiting the production of nitric oxide and pro-inflammatory cytokines via NF-κB and JNK pathways

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Abstract

Sea cucumber, Holothuria scabra, is an echinoderm marine animal that has long been used as a traditional therapeutic in various diseases due to its chemical composition and protein enrichment. Many researchers have extensively studied the efficacy of sea cucumber extracts for many health benefits in recent years. Inflammation is a complex process involved in pro-/anti-inflammatory cytokine products. However, the role of the H. scabra extracts in anti-inflammation and its molecular regulations has not been apparently elucidated yet. In this study, we investigated the anti-inflammatory effect of H. scabra extracts by using lipopolysaccharide (LPS) from E. coli to induce an inflammatory response in RAW264.7 macrophage. It was found that ethyl acetate fraction of H. scabra extracts (EAHS) inhibited pro-inflammatory cytokines synthesis at both the transcriptional and translational levels, notably nitric oxide (NO), inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and prostaglandin E2 (PGE2). In addition, EAHS was able to downregulate IκB/NF-κB, and JNK expressions. These effects may be influenced by high contents of phenolic compound and triterpene glycosides in EAHS. Therefore, EAHS might have the potential to be developed as a natural anti-inflammatory agent.

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Acknowledgements

This work was supported by Agriculture Research Development Agency (Public Organization), Thailand to Prof. Prasert Sobhon, Research Fund, and the Central Instrument Facility (CIF) grant, Faculty of Science, Mahidol University, Bangkok, Thailand.

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Correspondence to Kulathida Chaithirayanon.

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Pranweerapaiboon, K., Apisawetakan, S., Nobsathian, S. et al. An ethyl-acetate fraction of Holothuria scabra modulates inflammation in vitro through inhibiting the production of nitric oxide and pro-inflammatory cytokines via NF-κB and JNK pathways. Inflammopharmacol 28, 1027–1037 (2020). https://doi.org/10.1007/s10787-019-00677-3

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  • DOI: https://doi.org/10.1007/s10787-019-00677-3

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