首页> 外文期刊>International Journal of Biological Macromolecules: Structure, Function and Interactions >Physicochemical characterization of polysaccharide from the leaf of Dendrobium officinale and effect on LPS induced damage in GES-1 cell
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Physicochemical characterization of polysaccharide from the leaf of Dendrobium officinale and effect on LPS induced damage in GES-1 cell

机译:从石斛offinale叶片的多糖的理化特征及对GES-1细胞LPS诱导损伤的影响

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The polysaccharide was first successfully isolated from the leaf of Dendrobium officinale by hot water extraction and alcohol predpitation and further purified using DEAE-52 and Sephadex G-100 chromatography. The structure of LDOP-1 was characterized by HPLC, GPC, and FT-IR and NMR spectroscopy, and its protective effect on LPS-induced GES-1 cell injury was analyzed. Results showed that LDOP was a homogeneous polysaccharide with average molecular weight of 91.8 kDa and consisted of Man, Gla, Glc, Glc add, and Ara at a molar ratio of 2.0:13:1.6:1.7:0.7. LDOP had two types of residues, including 1,6-linked alpha-D-Glup and 1,4-linked alpha-D-Manp. Activity studies indicated that LDOP-1 can significantly suppress the release of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and IL-6 from LPS-induced GES-1 cell injury, decreased the protein expressions of TLR4. phospho-NF-kappa B, ASC, NLRP3, cleaved-IL-1 beta, IL-6, and Bax, increased the protein expression of Bcl-2, and downregulated the ratios of cleaved caspase-1 to pro-caspase-1, phospho-I kappa B alpha to Ma, and phospho-NF-kappa B to NF kappa B. These findings strongly suggested that LDOP can prevent LPS-induced GES-1 cell injury by inhibiting the release of inflammatory cytokines regulated via the TLR4/NF-kappa B signal pathways. (C) 2020 Published by Elsevier B.V.
机译:首先通过热水萃取和酒精灌注从石斛officinale的叶子成功分离多糖,并使用DEAE-52和Sephadex G-100色谱法进一步纯化。 LDOP-1的结构的特征在于HPLC,GPC和FT-IR和NMR光谱,分析了对LPS诱导的GES-1细胞损伤的保护作用。结果表明,LDOP是一个均匀的多糖,平均分子量为91.8kDa,由MAN,GLA,GLC,GLC添加和ARA以2.0:13:1.6:1.7:0.7的摩尔比组成。 LDOP有两种类型的残留物,包括1,6-连接的α-D-GLUP和1,4-连接的α-D-MANP。活动研究表明,LDOP-1可以显着抑制肿瘤坏死因子-α(TNF-α),白细胞介素-1β(IL-1β)和IL-6的释放,来自LPS诱导的GES-1细胞损伤,降低TLR4的蛋白质表达。磷酸NF-Kappa B,ASC,NLRP3,切割-IL-1β,IL-6和Bax增加了Bcl-2的蛋白质表达,并将切割的Caspase-1的比例下调至pro-caspase-1,磷酸-1 kappabαa至ma,磷酸-nf-κb至nf kappa b.这些结果强烈建议LDOP通过抑制通过TLR4 / NF调节的炎性细胞因子的释放可以防止LPS诱导的GES-1细胞损伤-Kappa B信号路径。 (c)2020由elsevier b.v发布。

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