Dendrobium officinale polysaccharides protected against ethanol-induced acute liver injury in vivo and in vitro via the TLR4/NF-κB signaling pathway.

Dendrobium officinale polysaccharides protected against ethanol-induced acute liver injury in vivo and in vitro via the TLR4/NF-κB signaling pathway.
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DOI:
10.1016/j.cyto.2020.155058
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发表时间:
2020-03
期刊:
影响因子:
3.8
通讯作者:
Ke Yang;Lianghui Zhan;Tingting Lu;Cong Zhou;Xue Chen;Ying-Jie Dong;Guiyuan Lv;Suhong Chen
Ke Yang;Lianghui Zhan;Tingting Lu;Cong Zhou;Xue Chen;Ying-Jie Dong;Guiyuan Lv;Suhong Chen
中科院分区:
医学3区
文献类型:
--
作者:
Ke Yang;Lianghui Zhan;Tingting Lu;Cong Zhou;Xue Chen;Ying-Jie Dong;Guiyuan Lv;Suhong Chen

文献摘要

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酒精性肝损伤的特点是强烈的炎症反应。从中草药中分离的多糖对乙醇诱导的肝损伤有保护作用。是一种含有一定量多糖的新型食品资源。然而,D.药用多糖(DOP)仍然未知。因此,本研究旨在评估体内和体外DOP的肝保护作用和潜在机制。雄性Sprague-Dawley大鼠经口给予DOP(400和100 mg/kg)30 d后,灌胃无水乙醇(5 mL/kg)建立酒精性肝损伤模型。苏木精-伊红染色用于肝细胞变性的组织学评估,并测量血清和肝组织中的AST和ALT水平。采用ELISA和免疫组织化学方法评价炎症标志物。进一步探讨了DOP在酒精诱导的肝细胞损伤中的作用机制。结果表明,DOP能明显降低血清和肝组织中AST的含量,明显减少炎症细胞因子IL-1β、IL-6和TNF-α的产生,并能有效抑制NF-κB的磷酸化。体外实验表明,DOP可显著提高LO 2细胞的存活率,抑制LDH的释放,减少IL-1β、IL-6、TNF-α的分泌,逆转IL-1β、IL-6、TNF-α、caspase 1、NLRP 3、p-NF-κB、TLR 4的表达。结论:DOP可通过TLR 4/NF-κB信号通路减轻乙醇诱导的急性肝损伤。
Alcohol-induced liver injury is characterized by strong inflammation. Polysaccharides separated from herbs can prevent ethanol-induced liver injury.Dendrobium officinaleKimura et Migo leaves (D. officinale) are a new food resource that contains a certain amount of polysaccharide. However, the hepatoprotective effects and the potential mechanisms ofD. officinale polysaccharide(DOP) remain unknown. Thus, this study aimed to assess the hepatoprotective effects and potential mechanism invivoand invitroof DOP. Male Sprague–Dawley rats were used to establish alcohol-induced liver injury models through the oral gavage of absolute alcohol (5 mL/kg) after the oral administration of DOP (400 and 100 mg/kg) for 30 days. Hematoxylin–eosin staining was used for the histological assessments of hepatocyte degeneration, and the AST and ALT levels in the serum and liver tissue were measured. The inflammatory markers were evaluated using ELISA and immunohistochemistry. The potential mechanism of DOP in alcohol-induced liver cell (LO2) injury in vitro was further identified. Results showed that DOP clearly decreased the AST in the serum and hepatic tissue, obviously reduced the production of inflammatory cytokines (such as IL-1β, IL-6, and TNF-α), and can successfully inhibit NF-κB phosphorylation in vivo. In vitro experiments indicated that DOP increased the LO2cell viability; prevented LDH release prominently; reduced the secretion of IL-1β, IL-6, and TNF-α; and reversed the expression of IL-1β, IL-6, TNF-α, caspase 1, NLRP3, p-NF-κB, and TLR4. Overall, DOP can alleviate ethanol-induced acute liver injury via the TLR4/NF-κB signaling pathway.