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Green tea polysaccharide-conjugates protect human umbilical vein endothelial cells against impairments triggered by high glucose

Green tea polysaccharide-conjugates protect human umbilical vein endothelial cells against impairments triggered by high glucose,10.1016/j.ijbiomac.20

Green tea polysaccharide-conjugates protect human umbilical vein endothelial cells against impairments triggered by high glucose  
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Hot-water extracts of low-grade green tea were precipitated with ethanol, deproteinized with trichloroacetic acid, neutralized with NaOH and fractionated by DEAE-cellulose DE-52 column chromatography to yield three (3) of unexplored polysaccharide-conjugate fractions termed gTPC1, gTPC2 and gTPC3. Monosaccharide and amino acid composition, contents of total neutral sugars, proteins and moistures, HPGPC distribution and Zeta potentials of gTPC1–3 were investigated. Exposure of human umbilical vein endothelial (HUVE) cells to high glucose (33mM) for 12h significantly decreased cell viability relative to normal glucose control (p<0.001). As compared with cell injury group, gTPC1–3 at all of three dose levels (50, 150 and 300μg/mL) were found to possess remarkably protective effects on HUVE cells against impairments induced by high glucose in a dose-dependent manner (p<0.05, p<0.001). To contribute toward our understanding of the cell-based protection mechanism of gTPC1–3, the latter were subjected to self-oxidation of 1,2,3-phentriol assay, and their scavenging effects were observed as 55.1%, 47.6% and 47.9% at the concentration of 300μg/mL, respectively. On the basis of the fact that high glucose-induced endothelial dysfunction involves in the overproduction of reactive oxygen species (ROS) and contributes to the vascular complications in patients with diabetes, inhibitory effects of gTPC1–3 on high glucose-mediated HUVE cell loss are, at least in part, correlated with their potential scavenging potency of ROS. Taken together, gTPC1–3 could be developed as non-cytotoxic candidates of therapeutic agent for diabetic vascular complications.
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