[Antagonism of LY333531 on high glucose induced permeability upregulation of cardiac microvascular endothelial cells]

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2009 Apr;25(4):303-5.
[Article in Chinese]

Abstract

Aim: To investigate the antagonism of LY333531 on the increased permeability of cardiac microvascular endothelial cells (CMECs) induced by high glucose.

Methods: The cultured CMECs from rats were randomly divided into four groups: normal group, high glucose group (25 mmol/L), high glucose+LY333531 (10 micromol/L) group and high glucose+saline group. The permeability of cell monolayer was detected using in vitro vascular permeability assay kit. Cell apoptosis was determined by TUNEL and the expression of PKCbeta II was analyzed by immunofluorescence and Western blot in each group.

Results: Compared with normal group, the permeability (400.0+/-20.00 vs 223.3+/-25.17; P<0.01) of cell monolayer cultured in high glucose medium was increased at a higher apoptosis rate (55.00%+/-5.000% vs 2.333%+/-1.155%; P<0.01) and PKCbeta II expression (0.4767+/-0.0751 vs 0.1733+/-0.0208; P<0.01). However, the high glucose+LY333531 group showed noticeable attenuation on both permeability (360+/-17.32 vs 400.0+/-20.00; P<0.05) and apoptosis (25.00%+/-5.000% vs 55.00%+/-5.000%; P<0.01) with reduced PKCbeta II expression (0.2800+/-0.0700 vs 0.4767+/-0.0751; P<0.01). No significant effects of saline on the cell permeability, apoptosis and PKCbeta II expression were observed.

Conclusion: The antagonism of LY333531 has shown obvious effects on the impairment of high glucose to the permeability of CMECs.

Publication types

  • English Abstract

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Blotting, Western
  • Capillary Permeability / drug effects*
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Drug Synergism
  • Endothelial Cells / cytology
  • Endothelial Cells / drug effects*
  • Endothelial Cells / metabolism
  • Enzyme Inhibitors / pharmacology
  • Fluorescent Antibody Technique
  • Glucose / pharmacology*
  • In Situ Nick-End Labeling
  • Indoles / pharmacology*
  • Male
  • Maleimides / pharmacology*
  • Myocardium / cytology
  • Protein Kinase C / antagonists & inhibitors
  • Protein Kinase C / metabolism
  • Protein Kinase C beta
  • Rats
  • Rats, Sprague-Dawley
  • Up-Regulation / drug effects

Substances

  • Enzyme Inhibitors
  • Indoles
  • Maleimides
  • ruboxistaurin
  • Protein Kinase C
  • Protein Kinase C beta
  • Glucose