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Ethanol Extract ofAntrodia camphorataGrown on Germinated Brown Rice Suppresses Inflammatory Responses in Mice with Acute DSS-Induced Colitis
Author(s) -
Dong Ki Park,
Hye-Jin Park
Publication year - 2013
Publication title -
evidence-based complementary and alternative medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.552
H-Index - 90
eISSN - 1741-4288
pISSN - 1741-427X
DOI - 10.1155/2013/914524
Subject(s) - p38 mitogen activated protein kinases , tumor necrosis factor alpha , mapk/erk pathway , nitric oxide , lipopolysaccharide , in vivo , chemistry , nitric oxide synthase , ex vivo , prostaglandin e2 , colitis , in vitro , pharmacology , kinase , microbiology and biotechnology , biochemistry , immunology , medicine , biology , organic chemistry
The anti-inflammatory activity of Antrodia camphorata (AC) grown on germinated brown rice (CBR) extract was evaluated in vitro and in vivo . CBR suppressed the release of nitric oxide (NO) and prostaglandin (PG) E2 from lipopolysaccharide-(LPS-)stimulated RAW264.7 cells. CBR inhibited the level of inducible nitric oxide synthase (iNOS) and cyclooxygenase-(COX-)2 proteins, and it activated p38-MAPK, extracellular signal-related kinases (ERK), and NF- κ B in LPS-stimulated RAW264.7 macrophages. LPS-induced tumor necrosis factor- α (TNF- α ) and interleukin-6 (IL-6) mRNA expression was reduced in CBR-treated RAW264.7 cells. In concert with in vitro data, CBR suppressed the levels of dextran-sulfate-sodium-(DSS-)induced iNOS and COX-2 proteins in the colon tissue. CBR treatment inhibited activated p38-MAPK, ERK, and NF- κ B proteins in the colon tissue of DSS-induced mice. TNF- α and IL-6 mRNA expression was reduced in DSS+CBR-treated mice. The disease activity index and histological scores were significantly lower in CBR-treated mice (500 mg/kg/day) than in DSS-treated mice ( P < 0.05 versus DSS). This is the first report of anti-inflammatory activity of CBR in DSS-induced acute colitis. These results suggest that CBR is a promising, potential agent for preventing acute colitis through the inhibition of NF- κ B signaling and its upstream signaling molecules, including MAPKs.

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