4.7 Article

Physicochemical characterization of polysaccharide from the leaf of Dendrobium officinale and effect on LPS induced damage in GES-1 cell

Journal

INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
Volume 149, Issue -, Pages 320-330

Publisher

ELSEVIER
DOI: 10.1016/j.ijbiomac.2020.01.026

Keywords

Dendrobium officinale leaf; Polysaccharide; GES-1 cell; Inflammation

Funding

  1. National Key Research and Development Program [2017YFC1702200]
  2. National Science Foundation of China [81673638, 81874352, 81803761]
  3. Ten-thousand Talents Program of Zhejiang Province [ZJWR0102035]
  4. Funding for Young Talents Project of Zhejiang University of Technology [GY18034148004]
  5. China Postdoctoral Science Foundation [2019M652144]
  6. Zhejiang Provincial Natural Science Foundation of China [LQ17H280005]

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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.

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