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U‐bang‐haequi tang , an herbal prescription ameliorates acute inflammation through inhibition of NF‐kB in vivo and in vitro (LB550)
Author(s) -
Kim Sang Chan,
Jung Ji Yun,
Hwangbo Min,
Jee Seon Young,
Jegal Kyung Hwan,
Park Sang Mi,
Cho Il Je,
Kim Young Woo
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb550
Subject(s) - inflammation , in vivo , pharmacology , lipopolysaccharide , medicine , nitric oxide , iκbα , prostaglandin e2 , nf κb , immune system , immunology , biology , microbiology and biotechnology
Inflammation is a key response of the immune system to infection, and also a complex biological symptom of specific tissues to harmful injury, which is often caused by invading pathogens. U‐bang‐haequi tang (UBT) is an herbal prescription containing Arctii fructus and Forsythia suspensa as its main components. It has been used in traditional Korean medicine to treat a variety of diseases such as fever, infection, and inflammatory disorders. Although UBT has long been used as an herbal remedy, the underlying mechanism of its beneficial effects has not been clearly verified. This research investigated the effects of UBT against an acute phase of inflammation. We measured induction of both nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) expression as well as levels of related proteins in a lipopolysaccharide (LPS)‐stimulated macrophage cell line. Further, paw swelling was measured in carrageenan‐treated rats. Protein expression levels were determined by immunoblot analyses, and production of NO and PGE 2 was assessed by enzyme‐linked immunosorbent assay. Carrageenan treatment promoted infiltration of inflammatory cells and paw swelling, whereas oral administration of 0.3 or 1 g/kg/day of UBT inhibited the acute inflammatory response. UBT also inhibited mRNA and protein expression levels of iNOS. UBT treatment inhibited NO and PGE 2 production, nuclear accumulation of NF‐κB, and elevation of Iκ‐Bα phosphorylation, all of which were induced by LPS. Moreover, UBT treatment significantly blocked the ability of LPS to induce phosphorylation of p38 and c‐Jun NH2‐terminal kinases. In conclusion, UBT prevented both acute inflammation in rats as well as LPS‐induced NO and iNOS gene expression in RAW264.7 cells via inhibition of NF‐κB. Grant Funding Source : This work was supported by the National Research Foundation of Korea grant funded by the Korea government [MEST](No.2012‐0009400).