Quercetin prevents hepatic fibrosis by inhibiting hepatic stellate cell activation and reducing autophagy via the TGF-β1/Smads and PI3K/Akt pathways.

Quercetin prevents hepatic fibrosis by inhibiting hepatic stellate cell activation and reducing autophagy via the TGF-β1/Smads and PI3K/Akt pathways.
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槲皮素通过 TGF-β 1/Smads 和 PI3K/Akt 途径抑制肝星状细胞活化并减少自噬,从而预防肝纤维化

DOI:
10.1038/s41598-017-09673-5
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发表时间:
2017-08-24
期刊:
影响因子:
4.6
通讯作者:
Guo C
Guo C
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Wu L;Zhang Q;Mo W;Feng J;Li S;Li J;Liu T;Xu S;Wang W;Lu X;Yu Q;Chen K;Xia Y;Lu J;Xu L;Zhou Y;Fan X;Guo C

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本研究的目的是研究槲皮素对肝纤维化的影响,肝纤维化是急性或慢性肝损伤的特征性反应。将小鼠随机分为胆管结扎(BDL)或四氯化碳(CCl 4)肝硬化模型。槲皮素(每日100 mg/kg或200 mg/kg)灌胃给药2周或4周。收集肝组织和血液样品用于组织学和分子分析。我们的实验结果表明,槲皮素减少BDL或四氯化碳肝纤维化,抑制细胞外基质的形成,并调节基质金属肽酶(MMP)-9和金属蛋白酶组织抑制剂(TIMP)-1。槲皮素通过抑制TGF-β1/Smads信号通路和激活PI 3 K/Akt信号通路抑制BDL或CCl 4诱导的肝纤维化中的自噬来减轻肝损伤。槲皮素通过调节TGF-β1/Smads和PI 3 K/Akt通路之间的相互作用,抑制肝星状细胞活化,减少自噬,从而预防肝纤维化。
The aim of this study was to investigate the effect of quercetin on hepatic fibrosis, a characteristic response to acute or chronic liver injury. Mice were randomized to bile duct ligation (BDL) or carbon tetrachloride (CCl4) cirrhosis models. Quercetin (100 mg/kg or 200 mg/kg daily) was administered by gavage for 2 or 4 weeks. Liver tissue and blood samples were collected for histological and molecular analysis. The results of our experiments showed that quercetin reduced BDL or CCl4 liver fibrosis, inhibited extracellular matrix formation, and regulated matrix metallopeptidase (MMP)-9 and tissue inhibitor of metalloproteinase (TIMP)-1. Quercetin attenuated liver damage by suppressing the TGF-β1/Smads signaling pathway and activating the PI3K/Akt signaling pathway to inhibit autophagy in BDL- or CCl4- induced liver fibrosis. Quercetin prevented hepatic fibrosis by attenuating hepatic stellate cell activation and reducing autophagy through regulating crosstalk between the TGF-β1/Smads and PI3K/Akt pathways.
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发表时间: 2016-06-28
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作者:
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