Ethanol extract of Poria cocos reduces the production of inflammatory mediators by suppressing the NF-kappaB signaling pathway in lipopolysaccharide-stimulated RAW 264.7 macrophages

BMC Complementary and Alternative Medicine

Research Article

Jin-Woo Jeong¹  Yung Hyun Choi²  Min Ho Han²  Hye Hyeon Lee³  Cheol Park⁴  Gi-Young Kim⁵  Su Hyun Hong⁵ 

[1] Center for Core Research Facilities, Daegu Gyeongbuk Institute of Science & Technology, 711-873, Daegu, Republic of Korea;Department of Biochemistry, College of Oriental Medicine, Dongeui University, 614-052, Busan, Republic of Korea;Anti-Aging Research Center & Blue-Bio Industry RIC, Dongeui University, 614-714, Busan, Republic of Korea;Department of Biotechnology, College of Natural Resources and Life Science, Dong-A University, 604-714, Busan, Republic of Korea;Department of Molecular Biology, College of Natural Sciences, Dongeui University, 614-714, Busan, Republic of Korea;Laboratory of Immunobiology, Department of Marine Life Sciences, Jeju National University, 690-756, Jeju, Republic of Korea;

关键词: Poria cocos;    RAW 264.7 cells;    Anti-inflammation;    NF-κB;   

DOI  :  10.1186/1472-6882-14-101

 received in 2013-09-17, accepted in 2014-03-10,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundPoria cocos Wolf, a medicinal fungus, is widely used in traditional medicines in East Asian countries owing to its various therapeutic potentials. Although several studies have demonstrated the anti-inflammatory activity of this fungus, its underlying mechanisms have not yet been clearly defined.MethodsIn the present study, we have demonstrated the anti-inflammatory effects of ethanol extract of P. cocos (EEPC) in lipopolysaccaride (LPS)-stimulated RAW 264.7 macrophages. As inflammatory parameters, the productions of nitric oxide (NO), prostaglandin E2 (PGE2), interleukin (IL)-1β and tumor necrosis factor (TNF)-α were evaluated. We also examined the EEPC’s effect on the nuclear factor-kappaB (NF-κB) signaling pathway.ResultsOur results indicated that EEPC exhibits a potent inhibitory effect on NO production and inhibits PGE2 release in LPS-induced macrophages without affecting cell viability. EEPC also significantly attenuated LPS-induced secretion of inflammatory cytokines IL-1β and TNF-α. Additionally, LPS-induced expression of inducible NO synthase (iNOS), cyclooxygenase (COX)-2, IL-1β, and TNF-α was decreased by pre-treatment with EEPC at the transcriptional level. Moreover, EEPC clearly inhibited LPS-induced nuclear translocation of NF-κB p65 subunits, which correlated with EEPC’s inhibitory effects on inhibitor kappaB (IκB) degradation. Moreover, EEPC clearly suppressed the LPS-induced DNA-binding activity of NF-κB, as well as the nuclear translocation of the NF-κB p65, which correlated with EEPC’s inhibitory effects on inhibitor kappaB (IκB) degradation.ConclusionsTaken together, our data indicates that EEPC targets the inflammatory response of macrophages via inhibition of iNOS, COX-2, IL-1β, and TNF-α through inactivation of the NF-κB signaling pathway, supporting the pharmacological basis of P. cocos as a traditional herbal medicine for treatment of inflammation and its associated disorders.

【 授权许可】

Unknown   
© Jeong et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.