A plant kavalactone desmethoxyyangonin prevents inflammation and fulminant hepatitis in mice.
A plant kavalactone desmethoxyyangonin prevents inflammation and fulminant hepatitis in mice.
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DOI：
10.1371/journal.pone.0077626
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Shyur LF
中科院分区：
文献类型：
--
作者：
Chou TW;Feng JH;Huang CC;Cheng YW;Chien SC;Wang SY;Shyur LF
山姜是台湾特有的一种植物，被广泛用作治疗炎症和各种疾病的保健品或民间药物。本研究鉴定了植物根茎的活性化合物去甲氧基麻醉椒素（DMY），其对内毒素脂多糖（LPS）刺激的小鼠巨噬细胞炎症和LPS/D-半乳糖胺（LPS/D-GalN）诱导的小鼠暴发性肝炎具有新的作用。观察到DMY显著抑制离体T细胞的增殖和活化以及体外几种促炎介质的活性。DMY还通过抑制转氨酶活性和炎性巨噬细胞、中性粒细胞和致病性T细胞向肝组织的浸润来保护LPS/D-GalN−诱导的小鼠急性肝损伤。此外，与LPS/D-GalN −处理组（40%，4/10）相比，DMY预处理显著提高了LPS/D-GalN−处理小鼠的存活率至90%（9/10）。采用基于UPLC/MS平台的比较代谢组学方法，研究了DMY预处理前后暴发性肝衰竭（FHF）小鼠血清代谢谱的变化。结果表明，LPS/D-GalN−诱导的肝损伤可能是通过干扰氨基酸代谢，从而导致通过转氨酶催化的丙酮酸形成减少，DMY治疗可以在一定程度上预防LPS/D-GalN引起的小鼠代谢网络的这些改变。DMY对LPS或LPS/D-GalN−诱导的细胞或肝组织损伤具有保护作用，其机制主要是通过下调IKK/NFκB和Jak 2/STAT 3信号通路。本报告提供了基于证据的知识，以支持使用A的理由。葛根提取物的抗炎作用以及作为抗重症肝炎保肝药的新功能。
Alpinia pricei Hayata is a Formosan plant which has been popularly used as nutraceutical or folk medicine for inflammation and various disorders. An active compound of the plant rhizomes, desmethoxyyangonin (DMY), was identified in this study for its novel effect against endotoxin lipopolysaccharide (LPS)-stimulated inflammation in murine macrophages and LPS/D-galactosamine (LPS/D-GalN)-induced fulminant hepatitis in mice. DMY was observed to significantly inhibit proliferation and activation of T cells ex vivo and the activity of several pro-inflammatory mediators in vitro. DMY also protected LPS/D-GalN−induced acute hepatic damages in mice through inhibiting aminotransferases activities and infiltrations of inflammatory macrophages, neutrophils and pathogenic T cells into the liver tissues. In addition, pretreatment with DMY significantly improved the survival rate of LPS/D-GalN−treated mice to 90% (9/10), compared to LPS/D-GalN−treated group (40%, 4/10). UPLC/MS platform-based comparative metabolomics approach was used to explore the serum metabolic profile in fulminant hepatic failure (FHF) mice with or without the DMY pretreatment. The results showed that LPS/D-GalN−induced hepatic damage is likely through perturbing amino acid metabolism, which leads to decreased pyruvate formation via catalysis of aminotransferases, and DMY treatment can prevent to a certain degree of these alterations in metabolic network in mouse caused by LPS/D-GalN. Mechanistic investigation demonstrated that DMY protects LPS or LPS/D-GalN−induced damages in cell or liver tissues mainly through de-regulating IKK/NFκB and Jak2/STAT3 signaling pathways. This report provides evidence-based knowledge to support the rationale for the use of A. pricei root extract in anti-inflammation and also its new function as hepatoprotetive agent against fulminant hepatitis.
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影响因子：
5.6
作者：
Hou, Chia-Chung;Chen, Chun-Houh;Shyur, Lie-Fen
通讯作者：
Shyur, Lie-Fen
影响因子：
5.6
作者：
Huang, Chi-Chang;Lin, Kun-Ju;Shyur, Lie-Fen
通讯作者：
Shyur, Lie-Fen
影响因子：
13.5
作者：
Kosai, K;Matsumoto, K;Nakamura, T
通讯作者：
Nakamura, T
影响因子：
4.3
作者：
Chang, N. W.;Wu, C. T.;Lin, C. F.
通讯作者：
Lin, C. F.
影响因子：
4
作者：
Rawlings, JS;Rosler, KM;Harrison, DA
通讯作者：
Harrison, DA