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金钱草抑制炎症反应并改善脂多糖/D-氨基半乳糖诱导的肝损伤。

Lysimachiae Herba Inhibits Inflammatory Reactions and Improves Lipopolysaccharide/D-Galactosamine-Induced Hepatic Injury.

作者信息

Jeong Yun Hee, Kim Tae In, Oh You-Chang, Ma Jin Yeul

机构信息

Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine, 70 Cheomdanro, Dong-gu, Daegu 41062, Korea.

出版信息

Antioxidants (Basel). 2021 Aug 30;10(9):1387. doi: 10.3390/antiox10091387.

Abstract

This study aimed to determine the anti-inflammatory and hepatoprotective effects of Lysimachiae Herba ethanolic extract (LHE) in lipopolysaccharide (LPS)-stimulated macrophages and in a LPS/D-galactosamine (GalN)-induced acute hepatitis mouse model. Then, the production of inflammatory mediators and the activation of related pathways in macrophages were explored. Finally, we assessed the serum aminotransferase levels and the expression of inflammatory/antioxidant molecules in liver tissues in mice. Results revealed that LHE treatment significantly inhibited the production of inflammatory mediators in LPS-stimulated RAW 264.7 macrophages. Molecular data showed that LHE remarkably increased the activities of the antioxidant pathway and inhibited the phosphorylation of mitogen-activated protein kinase as well as the transcriptional activity of nuclear factor-κB induced by LPS. Furthermore, it prevented acute liver damage caused by LPS/D-GalN-induced hepatitis by inhibiting aminotransferase levels and histopathological changes in mice. Moreover, treatment with LHE significantly inhibited the activation of inflammatory pathways and increased the expression of antioxidant molecules including heme oxygenase-1/Nuclear factor erythroid 2-related factor 2. In conclusion, LHE has potent anti-inflammatory and hepatoprotective effects in LPS-stimulated macrophages and the LPS/D-GalN-induced acute hepatitis mouse model. Thus, it can be a treatment option for inflammation, hepatitis, and liver injury.

摘要

本研究旨在确定金钱草乙醇提取物(LHE)在脂多糖(LPS)刺激的巨噬细胞以及LPS/D-半乳糖胺(GalN)诱导的急性肝炎小鼠模型中的抗炎和肝保护作用。然后,探讨巨噬细胞中炎症介质的产生及相关信号通路的激活情况。最后,我们评估了小鼠血清转氨酶水平以及肝组织中炎症/抗氧化分子的表达。结果显示,LHE处理显著抑制了LPS刺激的RAW 264.7巨噬细胞中炎症介质的产生。分子数据表明,LHE显著增强了抗氧化信号通路的活性,并抑制了LPS诱导的丝裂原活化蛋白激酶的磷酸化以及核因子κB的转录活性。此外,它通过抑制小鼠的转氨酶水平和组织病理学变化,预防了LPS/D-GalN诱导的肝炎所导致的急性肝损伤。而且,LHE处理显著抑制了炎症信号通路的激活,并增加了包括血红素加氧酶-1/核因子红细胞2相关因子2在内的抗氧化分子的表达。总之,LHE在LPS刺激的巨噬细胞和LPS/D-GalN诱导的急性肝炎小鼠模型中具有强大的抗炎和肝保护作用。因此,它可以作为炎症、肝炎和肝损伤的一种治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/123e/8471683/94dd201dec35/antioxidants-10-01387-g001.jpg

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