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The effects of inhibiting the activation of hepatic stellate cells by lignan components from the fruits of Schisandra chinensis and the mechanism of schisanhenol.
Journal of Natural Medicines ( IF 2.5 ) Pub Date : 2020-03-19 , DOI: 10.1007/s11418-020-01394-w
Xiaoli He 1, 2, 3 , Jiamei Chen 1, 2 , Yongping Mu 1, 2 , Hua Zhang 1, 2 , Gaofeng Chen 1, 2 , Ping Liu 1, 2 , Wei Liu 1, 2
Affiliation  

Liver fibrosis is a pathological manifestation induced by chronic liver injury and may cause cirrhosis and liver cancer with the chronic progression of fibrosis. During the onset and progression of liver fibrosis, the activation of hepatic stellate cells (HSCs) is the core mechanism for the secretion of many extracellular matrices to induce fibrosis. Lignans are reportedly the main effective components of Schisandra chinensis with good anti-fibrosis effects. In this study, we compared the inhibiting effects of the seven lignan components from S. chinensis on HSC activation. We found that the seven lignans inhibited the activation of human HSCs (LX-2) in various degrees. Among all lignans, schisanhenol showed the best effect in inhibiting the activation of LX-2 with a dose–effect relationship. Sal also inhibited the phosphorylations of Smad1, Smad2, Smad3, extracellular regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), p38, and nuclear transcription factor-κB (NF-κB), as well as downregulated Smad4. All these findings suggested that schisanhenol may ameliorate liver fibrosis by inhibiting the transforming growth factor β (TGF-β)/Smad and mitogen-activated protein kinase (MAPK) signaling pathways. Remarkably, schisanhenol may be a potential anti-liver fibrosis drug and warrants further research.

中文翻译:

五味子果实中木脂素成分对肝星状细胞活化的抑制作用及五味子酚的作用机理。

肝纤维化是由慢性肝损伤引起的病理表现,随着肝纤维化的慢性发展,可能引起肝硬化和肝癌。在肝纤维化的发作和发展过程中,肝星状细胞(HSC)的激活是许多细胞外基质分泌引起纤维化的核心机制。据报道,木质素是五味子的主要有效成分,具有良好的抗纤维化作用。在这项研究中,我们比较了七种木脂多糖的抑制作用在HSC激活上。我们发现七个木脂素在不同程度上抑制了人类HSC(LX-2)的激活。在所有木脂素中,schisanhenol在抑制LX-2活化方面表现出最佳效果,且呈剂量-效应关系。Sal还抑制Smad1,Smad2,Smad3,细胞外调节蛋白激酶(ERK),c-Jun N末端激酶(JNK),p38和核转录因子-κB(NF-κB)的磷酸化,并下调Smad4。 。所有这些发现表明,五味子酚可以通过抑制转化生长因子β(TGF-β)/ Smad和有丝分裂原激活的蛋白激酶(MAPK)信号通路来改善肝纤维化。值得注意的是,五味子酚可能是潜在的抗肝纤维化药物,值得进一步研究。
更新日期:2020-03-19
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