Inviting an author to review:
Find an author and click ‘Invite to review selected article’ near their name.
Search for authorsSearch for similar articles
8
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Grape seed procyanidin B2 inhibits advanced glycation end product-induced endothelial cell apoptosis through regulating GSK3β phosphorylation.

      Cell Biology International
      Antigens, Surface, genetics, metabolism, Apoptosis, drug effects, Biflavonoids, pharmacology, therapeutic use, Blotting, Western, Caspase 3, Caspase Inhibitors, Catechin, Diabetes Mellitus, drug therapy, pathology, Endothelial Cells, cytology, Flow Cytometry, Gene Expression, Glycogen Synthase Kinase 3, antagonists & inhibitors, Glycosylation End Products, Advanced, adverse effects, Grape Seed Extract, Humans, Milk Proteins, Oxidative Stress, Phosphorylation, Polymerase Chain Reaction, Proanthocyanidins, Reactive Oxygen Species, Seeds, chemistry, Signal Transduction, Umbilical Veins, Vitis

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          To investigate the effects of GSPB2 (grape seed procyanidin B2) on the apoptosis of HUVECs (human umbilical endothelial cells) induced by AGEs (advanced glycation end products), HUVECs were treated with AGEs (200 μg/ml) in the presence or absence of GSPB2 (2.5, 5.0 and 10.0 μmol/l). Our findings showed that (i) AGEs induced HUVEC apoptosis and up-regulated the expression of caspase-3 activation and lactadherin and reduced the phosphorylation of GSK3β (glycogen synthase kinase 3β) at baseline. (ii) Treatment of HUVEC with GSPB2 significantly inhibited the cell apoptosis and the expression of caspase-3 activation and lactadherin induced by AGEs. Moreover, GSPB2 inhibited intracellular reactive oxygen species in a dose-dependent manner in AGEs-treated cells as determined by flow cytometry. (iii) GSPB2 increased the phosphorylation of GSK3β of HUVEC in response to AGEs. These findings suggest that the signalling pathway involving phosphorylation of GSK3β and lactadherin might play a key role in the endothelial apoptosis. GSPB2 therapy could become an effective approach to battling AGEs-induced endothelial apoptosis.

          Related collections

          Author and article information

          Comments

          Comment on this article