High glucose protects embryonic cardiac cells against simulated ischemia.
In the present study we investigated whether acute glucose administration could be protective against hypoxic stress. H9c2 cells were exposed to either 4.5 mM or 22 mM of glucose for 15,min and then were submitted to simulated ischemia. Cell death was microscopically assessed by combined staining with propidium iodide (PI) and Hoeschst 33358. Intracellular content of glucose was measured by enzymatic analysis. Clucose content of H9c2 cells was 48.24+/- 7.94 micromol/L in the 22 mM vs 23.86+/- 4.8 micromol/L in the 4.5 mM group (p < 0.05). PKCepsilon expression was increased 1.6 fold in the membrane fraction after pretreatment with high glucose (p < 0.05), while was decreased 1.6 fold in the cytosol (p < 0.05). In addition, no difference to PKCdelta translocation was observed after pretreatment with low glucose. After hypoxia, in the 22 mM group, cell death was found to be 17.36+/- 2.66% vs 38.2+/- 5.4% in the 4.5 mM group (p < 0.05). In the presence of iodoacetic acid, a glycolytic inhibitor, cell death was not different between the two groups (23.54+/- 3.2% in 22 mM vs 22.06+/- 5.3% in 4.5 mM). Addition of chelerythrine did not change the protective effect of high glucose (13.4+/- 1.7% cell death in 22 mM vs 27.5+/- 5.5% in 4.5 mM, p < 0.05). In conclusion, short pretreatment with high glucose protects H9c2 cells against hypoxia. Although this protective effect is associated with translocation of PKCepsilon and increased glucose uptake, it was abrogated only by inhibition of glycolysis.
Malliopoulou
Vassiliki
V
Department of Pharmacology, University of Athens, 75 Mikras Asias Ave., 11527 Goudi, Athens, Greece.
Xinaris
Christodoulos
C
Mourouzis
Iordanis
I
Cokkinos
Alexandros D
AD
Katsilambros
Nikolaos
N
Pantos
Constantinos
C
Kardami
Elissavet
E
Cokkinos
Dennis V
DV
D000818:Animals; D015687:Cell Hypoxia; D002460:Cell Line; D005947:Glucose / Q000378:metabolism* / Q000494:pharmacology; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000517:prevention & control; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism*; D010766:Phosphorylation; D051745:Protein Kinase C-delta / Q000378:metabolism; D051744:Protein Kinase C-epsilon / Q000378:metabolism; D021381:Protein Transport; D051381:Rats; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
D051745:Protein Kinase C-delta; D051744:Protein Kinase C-epsilon; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D048051:p38 Mitogen-Activated Protein Kinases; D005947:Glucose