首页> 美国卫生研究院文献>Evidence-based Complementary and Alternative Medicine : eCAM >Ethanol Extract of Antrodia camphorata Grown on Germinated Brown Rice Suppresses Inflammatory Responses in Mice with Acute DSS-Induced Colitis
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Ethanol Extract of Antrodia camphorata Grown on Germinated Brown Rice Suppresses Inflammatory Responses in Mice with Acute DSS-Induced Colitis

机译:发芽糙米上生长的樟脑樟脑乙醇提取物抑制急性DSS诱发的结肠炎小鼠的炎症反应。

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摘要

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-κB 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-κB 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-κB signaling and its upstream signaling molecules, including MAPKs.
机译:在体外和体内评价了在萌发的糙米(CBR)提取物中生长的樟脑樟芝(AC)的抗炎活性。 CBR抑制了脂多糖(LPS)刺激的RAW264.7细胞释放一氧化氮(NO)和前列腺素(PG)E2。 CBR抑制诱导型一氧化氮合酶(iNOS)和环氧合酶(COX-)2蛋白的水平,并激活LPS刺激的RAW264.7巨噬细胞中的p38-MAPK,细胞外信号相关激酶(ERK)和NF-κB。 。在经CBR处理的RAW264.7细胞中,LPS诱导的肿瘤坏死因子-α(TNF-α)和白介素6(IL-6)mRNA表达降低。与体外数据一致,CBR抑制了结肠组织中葡聚糖-硫酸钠-(DSS-)诱导的iNOS和COX-2蛋白的水平。 CBR处理可抑制DSS诱导的小鼠结肠组织中活化的p38-MAPK,ERK和NF-κB蛋白。 DSS + CBR处理的小鼠中TNF-α和IL-6 mRNA表达降低。 CBR治疗的小鼠(500μmg/ kg /天)的疾病活动指数和组织学评分显着低于DSS治疗的小鼠(P <0.05,相对于DSS)。这是CBR在DSS诱发的急性结肠炎中的抗炎活性的首次报道。这些结果表明,CBR是通过抑制NF- κ B信号及其上游信号分子(包括MAPKs)来预防急性结肠炎的一种有前途的潜在药物。

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