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Suppression of Inducible Nitric Oxide Synthase Expression by Nyasol and Broussonin A, Two Phenolic Compounds from Anemarrhena asphodeloides , through NF‐ κ B Transcriptional Regulation in vitro and in vivo
Author(s) -
Jin Lee Eun,
Chung HwaJin,
Pyee Yuna,
Hong JiYoung,
Joung Youn Ui,
Seo EunKyoung,
Kook Lee Sang
Publication year - 2014
Publication title -
chemistry and biodiversity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.427
H-Index - 70
eISSN - 1612-1880
pISSN - 1612-1872
DOI - 10.1002/cbdv.201400003
Subject(s) - nitric oxide synthase , chemistry , nitric oxide , protein kinase b , nf κb , mapk/erk pathway , lipopolysaccharide , in vivo , inflammation , pharmacology , p38 mitogen activated protein kinases , in vitro , iκbα , proinflammatory cytokine , signal transduction , biochemistry , biology , immunology , microbiology and biotechnology , organic chemistry
Anemarrhena asphodeloides is widely used in traditional Chinese medicine, and is known to possess antidiabetic and anti‐inflammatory properties. Because inducible nitric oxide synthase (iNOS) plays an important role in inflammation, we investigated the inhibitory effects of two known phenolic compounds, nyasol ( 1 ) and broussonin A ( 2 ), from A. asphodeloides , on iNOS and its plausible mechanism of action. Compounds 1 and 2 exhibited inhibitory effects on nitric oxide (NO) production in lipopolysaccharide (LPS)‐stimulated RAW 264.7 macrophage cells. Compounds 1 and 2 also suppressed the expressions of iNOS protein and mRNA. Moreover, compounds 1 and 2 suppressed the expression of inflammatory cytokines such as interleukin‐1 β (IL‐1 β ) and interferon‐ β (IFN‐ β ). They also inhibited the transcriptional activity of NF‐ κ B and degradation of I κ B‐ α , as well as the activation of Akt and ERK in LPS‐stimulated RAW 264.7 cells. In in vivo animal model, compounds 1 and 2 significantly inhibited TPA‐induced mouse ear edema. These results suggest that 1 and 2 suppress LPS‐stimulated iNOS expression at the transcriptional level through modulating NF‐ κ B and down‐regulation of the Akt and ERK signaling pathways. Taken together, these findings indicate that the suppressive effects of 1 and 2 on iNOS expression might provide one possible mechanism for their anti‐inflammatory activities.