Purpose: The results of the recent clinical trials on using cells as an additional therapeutic tool after myocardial infarct have clearly shown the need of more research on the possible mechanisms of actions. Our goal was to investigate if pluripotency of the used cells was an important factor and if cell therapy altered the formation of reactive oxygen species after ischemia. Methods: Vybrant DIO fluorescent-labeled H9c2 cardiomyoblasts were treated with oxygen-glucose deprivation (0.3% O2, OGD) for 2.5 hours, then no cells (OGD control), Vybrant DID-labeled healthy bone marrow derived mesenchymal stem cells (OGD +BMSC) or H9c2 cells (OGD+H9c2) were added 30 minutes after OGD and co-cultured. After 24 hours cell death was estimated using two methods: 1) the live-dead cell ratio using the dead-cell stain ethidium-homodimer analyzing confocal microscopic images with the help of the ImageJ software; 2) quantifying membrane disintegration using lactate dehydrogenase (LDH) assay with Triton-X treated cells as positive controls for 100% damage. To investigate the possible effects of H9c2 cell therapy on free radical formation we measured the concentration of the lipid peroxidation product malondialdehyde (MDA) 5 hours after OGD in the supernatant and in the cellular fraction as well. Results: Using the live-dead staining method the ratio of surviving cells significantly increased not only with pluripotent BMSCs, but with non-pluripotent H9c2 cells as well (OGD control: 17.2±5.2%; OGD+BMSC: 84.0±3.5%; OGD+H9c2: 43.5±9.6%). Measurements on membrane damage approximated by LDH assay showed that the H9c2 cell treatment significantly decreased the LDH levels in the supernatant from 38.6±10.1% to 8.6±3.8%. The MDA concentrations in the cellular fraction dropped to control levels with the addition of H9c2 cells (control: 0.75±0.43µM; OGD: 4.00±0.60µM; OGD+H9c2: 0.75±0.37µM), while in the supernatant the MDA level in the cell treated group decreased significantly (control: 0.47±0.18µM; OGD: 13.91±0.82µM; OGD+H9c2: 6.53±1.53µM). Conclusion: Addition of healthy, non-pluripotent cells to severly injured post-ischemic cardiomyoblasts can increase the number of surviving cells in an in vitro model. Our results indicate that: 1) pluripotency may not be completely necessary for cell therapy; 2) cell therapy leads to a decrease in the post-ischemic formation of reactive oxygen species. Funding: OTKA D45933, T049621, TET A4/04, TÁMOP 4.2.2-08/1/KMR-2008-0004.