Inhibition of LPS-induced inflammatory biomarkers by ethyl acetate fraction of Patrinia scabiosaefolia through suppression of NF-kB activation in RAW 264.7 cells

Title
Inhibition of LPS-induced inflammatory biomarkers by ethyl acetate fraction of Patrinia scabiosaefolia through suppression of NF-kB activation in RAW 264.7 cells
Authors
Lee Eun-JungKim ChulwonKim Jin-YoungKim Sung-MooNam DongwooJang Hyeung-JinKim Sung-HoonShim Bum SangAhn Kyoo SeokChoi SH정상훈Ahn Kwang Seok
Keywords
Patrinia scabiosaefolia; inflammation; NF-kB; nitric oxide; cyclooxygenase-2
Issue Date
2012-04
Publisher
Immunopharmacology and immunotoxicology
Citation
VOL 34, NO 2, 282-291
Abstract
Patrinia scabiosaefolia (PS) has been used for curing various types of inflammatory-related disorders. However, the precise mechanism of the anti-inflammatory activity of PS remains unclear. Here, we investigated the anti-inflammatory effects of several fractions isolated from the PS in RAW 264.7 macrophages. The results indicated that the ethyl acetate fraction of PS (EAPS) concentration highly suppressed lipopolysaccharide (LPS)-induced nitric oxide (NO) and IL-6 productions without a cytotoxic effect on RAW 264.7 cells. EAPS inhibited the expressions of LPS-induced iNOS and COX-2 protein and their mRNA in a dose-dependent manner. Particularly, EAPS suppressed the level of nuclear factor-κB (NF-κB) activity, which was linked with the suppression of LPS-induced phosphorylation of p65 at serine 276 and p65 translocation into nuclei, but not MAPK signaling. In addition, treatment with EAPS inhibited the production of TNF-α in LPS-injected mice and suppressed the production of IL-6 and TNF-α in LPS-stimulated splenocytes from BALB/c mice. Therefore, we demonstrate here that Patrinia scabiosaefolia potentially inhibits the biomarkers related to inflammation through the blocking of NF-κB p65 activation, and it may be a potential therapeutic candidate for the treatment of inflammatory diseases.
URI
http://pubs.kist.re.kr/handle/201004/42066
ISSN
08923973
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KIST Publication > Article
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