4.5 Article

The immune regulation of κ-carrageenan oligosaccharide and its desulfated derivatives on LPS-activated microglial cells

Journal

NEUROCHEMISTRY INTERNATIONAL
Volume 61, Issue 5, Pages 689-696

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2012.06.019

Keywords

Microglial Cell; kappa-Carrageenan oligosaccharides; Neurodegeneration disease; TNF-alpha; NO; IL-10

Funding

  1. National Natural Science Foundation of China [30901875, 81070973, 30970645]

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Neurodegenerative disease involves an inflammatory response in the central nervous system characterized by an increase in inflammatory cytokines and activation of microglial cell. To reveal the immune regulation activity of kappa-carrageenan oligosaccharides (KOS) on microglia cell activated by LPS and the relationship between the sulfate group content of KOS and its immune regulation activity, KOS was prepared by enzymatic hydrolysis. The degradation products of kappa-carrageenan were analyzed by high performance liquid chromatography (HPLC), ESI-TOF-MS and C-13 NMR spectroscopy, and the results indicated that the hydrolyzed products of the kappa-carrageenase were kappa-neocarrabiose-sulfate, kappa-neocarrahexaose-sulfate and kappa-neocarraoctaose-sulfate, respectively. Then desulfated derivatives of KOS (DSK) were obtained with DMSO-methanol-pyridine method. The effect of KOS and DSK on the viability of microglia cell activated by LPS was determined with MU method. Griess assay and ELISA method were used to determine the contents of NO/NO2-, TNF-alpha and IL-10 released by activated microglia cell, respectively. The results showed that KOS could inhibit the viability and content of NO, TNF-alpha and IL-10 released by LPS-activated microglia cell dose dependently. Compared with that of KOS, the inhibiting activity of DSK is weaker. So it could be concluded that KOS could protect microglial cell from being activated by LPS, and there was a positive relationship between the sulfate group content of KOS and its protection function. (C) 2012 Elsevier Ltd. All rights reserved.

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